https://embryology.med.unsw.edu.au/embryology/index.php?action=history&feed=atom&title=Abnormal_Development_-_ChemicalsAbnormal Development - Chemicals - Revision history2026-04-18T17:17:16ZRevision history for this page on the wikiMediaWiki 1.39.10https://embryology.med.unsw.edu.au/embryology/index.php?title=Abnormal_Development_-_Chemicals&diff=415818&oldid=prevZ8600021 at 00:02, 26 July 20202020-07-26T00:02:29Z<p></p>
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<tr><td class="diff-marker" data-marker="−"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div>* '''Environmental Influences and {{Polycystic <del style="font-weight: bold; text-decoration: none;">Ovarian </del>Syndrome}}'''{{#pmid:32701518|PMID32701518}} "Polycystic ovarian syndrome ({{PCOS}}) is a complex endocrine-metabolic disorder whose pathogenesis is not well-understood. While genetic insults have been hypothesized as possible causes, there are a large number of environmental chemicals known to have detrimental effects on the endocrine system and may be irreversible, especially when exposure occurs early in development. Many of these chemicals have been investigated as causes of PCOS by measuring serum and urinary levels of common endocrine disruptors in women and adolescents with PCOS as well as using animal models for PCOS induction with chemical exposures."</div></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div>* '''Environmental Influences and {{Polycystic <ins style="font-weight: bold; text-decoration: none;">Ovary </ins>Syndrome}}'''{{#pmid:32701518|PMID32701518}} "Polycystic ovarian syndrome ({{PCOS}}) is a complex endocrine-metabolic disorder whose pathogenesis is not well-understood. While genetic insults have been hypothesized as possible causes, there are a large number of environmental chemicals known to have detrimental effects on the endocrine system and may be irreversible, especially when exposure occurs early in development. Many of these chemicals have been investigated as causes of PCOS by measuring serum and urinary levels of common endocrine disruptors in women and adolescents with PCOS as well as using animal models for PCOS induction with chemical exposures."</div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>* '''The Impact of Di-2-Ethylhexyl Phthalate on Sperm Fertility'''{{#pmid:32695775|PMID32695775}} "A growing number of studies point to reduced fertility upon chronic exposure to endocrine-disrupting chemicals (EDCs) such as phthalates and plasticizers. These toxins are ubiquitous and are often found in food and beverage containers, medical devices, as well as in common household and personal care items. Animal studies with EDCs, such as phthalates and bisphenol A have shown a dose-dependent decrease in fertility and embryo toxicity upon chronic exposure. However, limited research has been conducted on the acute effects of these EDCs on male fertility. Here we used a murine model to test the acute effects of four ubiquitous environmental toxins: bisphenol A (BPA), di-2-ethylhexyl phthalate (DEHP), diethyl phthalate (DEP), and dimethyl phthalate (DMP) on sperm fertilizing ability and pre-implantation embryo development. The most potent of these toxins, di-2-ethylhexyl phthalate (DEHP), was further evaluated for its effect on sperm ion channel activity, capacitation status, acrosome reaction and generation of reactive oxygen species (ROS). DEHP demonstrated a profound hazardous effect on {{sperm}} fertility by producing an altered capacitation profile, impairing the {{acrosome}} reaction, and, interestingly, also increasing ROS production. These results indicate that in addition to its known chronic impact on reproductive potential, DEHP also imposes acute and profound damage to spermatozoa, and thus, represents a significant risk to male fertility."</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>* '''The Impact of Di-2-Ethylhexyl Phthalate on Sperm Fertility'''{{#pmid:32695775|PMID32695775}} "A growing number of studies point to reduced fertility upon chronic exposure to endocrine-disrupting chemicals (EDCs) such as phthalates and plasticizers. These toxins are ubiquitous and are often found in food and beverage containers, medical devices, as well as in common household and personal care items. Animal studies with EDCs, such as phthalates and bisphenol A have shown a dose-dependent decrease in fertility and embryo toxicity upon chronic exposure. However, limited research has been conducted on the acute effects of these EDCs on male fertility. Here we used a murine model to test the acute effects of four ubiquitous environmental toxins: bisphenol A (BPA), di-2-ethylhexyl phthalate (DEHP), diethyl phthalate (DEP), and dimethyl phthalate (DMP) on sperm fertilizing ability and pre-implantation embryo development. The most potent of these toxins, di-2-ethylhexyl phthalate (DEHP), was further evaluated for its effect on sperm ion channel activity, capacitation status, acrosome reaction and generation of reactive oxygen species (ROS). DEHP demonstrated a profound hazardous effect on {{sperm}} fertility by producing an altered capacitation profile, impairing the {{acrosome}} reaction, and, interestingly, also increasing ROS production. These results indicate that in addition to its known chronic impact on reproductive potential, DEHP also imposes acute and profound damage to spermatozoa, and thus, represents a significant risk to male fertility."</div></td></tr>
</table>Z8600021https://embryology.med.unsw.edu.au/embryology/index.php?title=Abnormal_Development_-_Chemicals&diff=415816&oldid=prevZ8600021 at 00:01, 26 July 20202020-07-26T00:01:27Z<p></p>
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<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>* '''Environmental Influences and {{Polycystic Ovarian Syndrome}}'''{{#pmid:32701518|PMID32701518}} "Polycystic ovarian syndrome ({{PCOS}}) is a complex endocrine-metabolic disorder whose pathogenesis is not well-understood. While genetic insults have been hypothesized as possible causes, there are a large number of environmental chemicals known to have detrimental effects on the endocrine system and may be irreversible, especially when exposure occurs early in development. Many of these chemicals have been investigated as causes of PCOS by measuring serum and urinary levels of common endocrine disruptors in women and adolescents with PCOS as well as using animal models for PCOS induction with chemical exposures."</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>* '''Environmental Influences and {{Polycystic Ovarian Syndrome}}'''{{#pmid:32701518|PMID32701518}} "Polycystic ovarian syndrome ({{PCOS}}) is a complex endocrine-metabolic disorder whose pathogenesis is not well-understood. While genetic insults have been hypothesized as possible causes, there are a large number of environmental chemicals known to have detrimental effects on the endocrine system and may be irreversible, especially when exposure occurs early in development. Many of these chemicals have been investigated as causes of PCOS by measuring serum and urinary levels of common endocrine disruptors in women and adolescents with PCOS as well as using animal models for PCOS induction with chemical exposures."</div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;"></ins></div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">* '''The Impact of Di-2-Ethylhexyl Phthalate on Sperm Fertility'''{{#pmid:32695775|PMID32695775}} "A growing number of studies point to reduced fertility upon chronic exposure to endocrine-disrupting chemicals (EDCs) such as phthalates and plasticizers. These toxins are ubiquitous and are often found in food and beverage containers, medical devices, as well as in common household and personal care items. Animal studies with EDCs, such as phthalates and bisphenol A have shown a dose-dependent decrease in fertility and embryo toxicity upon chronic exposure. However, limited research has been conducted on the acute effects of these EDCs on male fertility. Here we used a murine model to test the acute effects of four ubiquitous environmental toxins: bisphenol A (BPA), di-2-ethylhexyl phthalate (DEHP), diethyl phthalate (DEP), and dimethyl phthalate (DMP) on sperm fertilizing ability and pre-implantation embryo development. The most potent of these toxins, di-2-ethylhexyl phthalate (DEHP), was further evaluated for its effect on sperm ion channel activity, capacitation status, acrosome reaction and generation of reactive oxygen species (ROS). DEHP demonstrated a profound hazardous effect on {{sperm}} fertility by producing an altered capacitation profile, impairing the {{acrosome}} reaction, and, interestingly, also increasing ROS production. These results indicate that in addition to its known chronic impact on reproductive potential, DEHP also imposes acute and profound damage to spermatozoa, and thus, represents a significant risk to male fertility."</ins></div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>* '''Prenatal exposure to organophosphate pesticides and functional neuroimaging in adolescents living in proximity to pesticide application'''{{#pmid:31451641|PMID31451641}} "We have reported consistent associations of prenatal organophosphate pesticide (OP) exposure with poorer cognitive function and behavior problems in our Center for the Health Assessment of Mothers and Children of Salinas (CHAMACOS), a birth cohort of Mexican American youth in California's agricultural Salinas Valley. However, there is little evidence on how OPs affect neural dynamics underlying associations. We used functional near-infrared spectroscopy (fNIRS) to measure cortical activation during tasks of executive function, attention, social cognition, and language comprehension in 95 adolescent CHAMACOS participants. We estimated associations of residential proximity to OP use during pregnancy with cortical activation in frontal, temporal, and parietal regions using multiple regression models, adjusting for sociodemographic characteristics. OP exposure was associated with altered brain activation during tasks of executive function. For example, with a 10-fold increase in total OP pesticide use within 1 km of maternal residence during pregnancy, there was a bilateral decrease in brain activation in the prefrontal cortex during a cognitive flexibility task (β = -4.74; 95% CI: -8.18, -1.31 and β = -4.40; 95% CI: -7.96, -0.84 for the left and right hemispheres, respectively). We also found that prenatal OP exposure was associated with sex differences in brain activation during a language comprehension task. This first functional neuroimaging study of prenatal OP exposure suggests that pesticides may impact cortical brain activation, which could underlie previously reported OP-related associations with cognitive and behavioral function. Use of fNIRS in environmental epidemiology offers a practical alternative to neuroimaging technologies and enhances our efforts to assess the impact of chemical exposures on neurodevelopment." {{neural abnormalities}}</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>* '''Prenatal exposure to organophosphate pesticides and functional neuroimaging in adolescents living in proximity to pesticide application'''{{#pmid:31451641|PMID31451641}} "We have reported consistent associations of prenatal organophosphate pesticide (OP) exposure with poorer cognitive function and behavior problems in our Center for the Health Assessment of Mothers and Children of Salinas (CHAMACOS), a birth cohort of Mexican American youth in California's agricultural Salinas Valley. However, there is little evidence on how OPs affect neural dynamics underlying associations. We used functional near-infrared spectroscopy (fNIRS) to measure cortical activation during tasks of executive function, attention, social cognition, and language comprehension in 95 adolescent CHAMACOS participants. We estimated associations of residential proximity to OP use during pregnancy with cortical activation in frontal, temporal, and parietal regions using multiple regression models, adjusting for sociodemographic characteristics. OP exposure was associated with altered brain activation during tasks of executive function. For example, with a 10-fold increase in total OP pesticide use within 1 km of maternal residence during pregnancy, there was a bilateral decrease in brain activation in the prefrontal cortex during a cognitive flexibility task (β = -4.74; 95% CI: -8.18, -1.31 and β = -4.40; 95% CI: -7.96, -0.84 for the left and right hemispheres, respectively). We also found that prenatal OP exposure was associated with sex differences in brain activation during a language comprehension task. This first functional neuroimaging study of prenatal OP exposure suggests that pesticides may impact cortical brain activation, which could underlie previously reported OP-related associations with cognitive and behavioral function. Use of fNIRS in environmental epidemiology offers a practical alternative to neuroimaging technologies and enhances our efforts to assess the impact of chemical exposures on neurodevelopment." {{neural abnormalities}}</div></td></tr>
</table>Z8600021https://embryology.med.unsw.edu.au/embryology/index.php?title=Abnormal_Development_-_Chemicals&diff=415812&oldid=prevZ8600021 at 23:56, 25 July 20202020-07-25T23:56:25Z<p></p>
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<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">* '''Environmental Influences and {{Polycystic Ovarian Syndrome}}'''{{#pmid:32701518|PMID32701518}} "Polycystic ovarian syndrome ({{PCOS}}) is a complex endocrine-metabolic disorder whose pathogenesis is not well-understood. While genetic insults have been hypothesized as possible causes, there are a large number of environmental chemicals known to have detrimental effects on the endocrine system and may be irreversible, especially when exposure occurs early in development. Many of these chemicals have been investigated as causes of PCOS by measuring serum and urinary levels of common endocrine disruptors in women and adolescents with PCOS as well as using animal models for PCOS induction with chemical exposures."</ins></div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;"></ins></div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>* '''Prenatal exposure to organophosphate pesticides and functional neuroimaging in adolescents living in proximity to pesticide application'''{{#pmid:31451641|PMID31451641}} "We have reported consistent associations of prenatal organophosphate pesticide (OP) exposure with poorer cognitive function and behavior problems in our Center for the Health Assessment of Mothers and Children of Salinas (CHAMACOS), a birth cohort of Mexican American youth in California's agricultural Salinas Valley. However, there is little evidence on how OPs affect neural dynamics underlying associations. We used functional near-infrared spectroscopy (fNIRS) to measure cortical activation during tasks of executive function, attention, social cognition, and language comprehension in 95 adolescent CHAMACOS participants. We estimated associations of residential proximity to OP use during pregnancy with cortical activation in frontal, temporal, and parietal regions using multiple regression models, adjusting for sociodemographic characteristics. OP exposure was associated with altered brain activation during tasks of executive function. For example, with a 10-fold increase in total OP pesticide use within 1 km of maternal residence during pregnancy, there was a bilateral decrease in brain activation in the prefrontal cortex during a cognitive flexibility task (β = -4.74; 95% CI: -8.18, -1.31 and β = -4.40; 95% CI: -7.96, -0.84 for the left and right hemispheres, respectively). We also found that prenatal OP exposure was associated with sex differences in brain activation during a language comprehension task. This first functional neuroimaging study of prenatal OP exposure suggests that pesticides may impact cortical brain activation, which could underlie previously reported OP-related associations with cognitive and behavioral function. Use of fNIRS in environmental epidemiology offers a practical alternative to neuroimaging technologies and enhances our efforts to assess the impact of chemical exposures on neurodevelopment." {{neural abnormalities}}</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>* '''Prenatal exposure to organophosphate pesticides and functional neuroimaging in adolescents living in proximity to pesticide application'''{{#pmid:31451641|PMID31451641}} "We have reported consistent associations of prenatal organophosphate pesticide (OP) exposure with poorer cognitive function and behavior problems in our Center for the Health Assessment of Mothers and Children of Salinas (CHAMACOS), a birth cohort of Mexican American youth in California's agricultural Salinas Valley. However, there is little evidence on how OPs affect neural dynamics underlying associations. We used functional near-infrared spectroscopy (fNIRS) to measure cortical activation during tasks of executive function, attention, social cognition, and language comprehension in 95 adolescent CHAMACOS participants. We estimated associations of residential proximity to OP use during pregnancy with cortical activation in frontal, temporal, and parietal regions using multiple regression models, adjusting for sociodemographic characteristics. OP exposure was associated with altered brain activation during tasks of executive function. For example, with a 10-fold increase in total OP pesticide use within 1 km of maternal residence during pregnancy, there was a bilateral decrease in brain activation in the prefrontal cortex during a cognitive flexibility task (β = -4.74; 95% CI: -8.18, -1.31 and β = -4.40; 95% CI: -7.96, -0.84 for the left and right hemispheres, respectively). We also found that prenatal OP exposure was associated with sex differences in brain activation during a language comprehension task. This first functional neuroimaging study of prenatal OP exposure suggests that pesticides may impact cortical brain activation, which could underlie previously reported OP-related associations with cognitive and behavioral function. Use of fNIRS in environmental epidemiology offers a practical alternative to neuroimaging technologies and enhances our efforts to assess the impact of chemical exposures on neurodevelopment." {{neural abnormalities}}</div></td></tr>
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</table>Z8600021https://embryology.med.unsw.edu.au/embryology/index.php?title=Abnormal_Development_-_Chemicals&diff=415804&oldid=prevZ8600021 at 23:44, 25 July 20202020-07-25T23:44:53Z<p></p>
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<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">{{#pmid:32707888}}</ins></div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;"></ins></div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>{{#pmid:18470797}}</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>{{#pmid:18470797}}</div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;"></ins></div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>===Articles===</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>===Articles===</div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>{{#pmid:19683226}}</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>{{#pmid:19683226}}</div></td></tr>
</table>Z8600021https://embryology.med.unsw.edu.au/embryology/index.php?title=Abnormal_Development_-_Chemicals&diff=390502&oldid=prevZ8600021 at 22:36, 19 November 20192019-11-19T22:36:38Z<p></p>
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<td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">Revision as of 08:36, 20 November 2019</td>
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<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>|</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>|</div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">* '''Prenatal exposure to organophosphate pesticides and functional neuroimaging in adolescents living in proximity to pesticide application'''{{#pmid:31451641|PMID31451641}} "We have reported consistent associations of prenatal organophosphate pesticide (OP) exposure with poorer cognitive function and behavior problems in our Center for the Health Assessment of Mothers and Children of Salinas (CHAMACOS), a birth cohort of Mexican American youth in California's agricultural Salinas Valley. However, there is little evidence on how OPs affect neural dynamics underlying associations. We used functional near-infrared spectroscopy (fNIRS) to measure cortical activation during tasks of executive function, attention, social cognition, and language comprehension in 95 adolescent CHAMACOS participants. We estimated associations of residential proximity to OP use during pregnancy with cortical activation in frontal, temporal, and parietal regions using multiple regression models, adjusting for sociodemographic characteristics. OP exposure was associated with altered brain activation during tasks of executive function. For example, with a 10-fold increase in total OP pesticide use within 1 km of maternal residence during pregnancy, there was a bilateral decrease in brain activation in the prefrontal cortex during a cognitive flexibility task (β = -4.74; 95% CI: -8.18, -1.31 and β = -4.40; 95% CI: -7.96, -0.84 for the left and right hemispheres, respectively). We also found that prenatal OP exposure was associated with sex differences in brain activation during a language comprehension task. This first functional neuroimaging study of prenatal OP exposure suggests that pesticides may impact cortical brain activation, which could underlie previously reported OP-related associations with cognitive and behavioral function. Use of fNIRS in environmental epidemiology offers a practical alternative to neuroimaging technologies and enhances our efforts to assess the impact of chemical exposures on neurodevelopment." {{neural abnormalities}}</ins></div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;"></ins></div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>* '''Review - A mechanism for the effect of endocrine disrupting chemicals on placentation'''{{#pmid:31132539|PMID31132539}} "Numerous recent studies have shown that endocrine disrupting chemicals (EDCs) in the body of pregnant women can pass through the placenta and be exposed to the fetus, leading to fetal development and cognitive impairment. Placentation through invasion of trophoblast cells and vascular remodeling is essential to maintaining maternal and fetal health throughout the pregnancy. Abnormal placentation can lead to pregnancy disorders such as preeclampsia (PE) and intrauterine growth retardation (IUGR). However, many studies have not been conducted on whether EDCs can inhibit the development and function of the placenta. Isolating placental tissues to analyze the effect of EDCs on placentation has several limitations. In this review, we discussed the types of EDCs that can pass through the placental barrier and accumulate in the placenta with relative outcome. EDCs can be released from a variety of products including plasticizers, pesticides, and retardant. We also discussed the development and dysfunction of the placenta when EDCs were treated on trophoblast cells or pregnant rodent models. The effects of EDCs on the placenta of livestock are also discussed, together with the molecular mechanism of EDCs acting in trophoblast cells. We describe how EDCs cross the membrane of trophoblasts to regulate signaling pathways, causing genetic and epigenetic changes that lead to changes in cell viability and invasiveness. Further studies on the effects of EDCs on placenta may draw attention to the correct use of products containing EDCs during pregnancy." {{placenta}}</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>* '''Review - A mechanism for the effect of endocrine disrupting chemicals on placentation'''{{#pmid:31132539|PMID31132539}} "Numerous recent studies have shown that endocrine disrupting chemicals (EDCs) in the body of pregnant women can pass through the placenta and be exposed to the fetus, leading to fetal development and cognitive impairment. Placentation through invasion of trophoblast cells and vascular remodeling is essential to maintaining maternal and fetal health throughout the pregnancy. Abnormal placentation can lead to pregnancy disorders such as preeclampsia (PE) and intrauterine growth retardation (IUGR). However, many studies have not been conducted on whether EDCs can inhibit the development and function of the placenta. Isolating placental tissues to analyze the effect of EDCs on placentation has several limitations. In this review, we discussed the types of EDCs that can pass through the placental barrier and accumulate in the placenta with relative outcome. EDCs can be released from a variety of products including plasticizers, pesticides, and retardant. We also discussed the development and dysfunction of the placenta when EDCs were treated on trophoblast cells or pregnant rodent models. The effects of EDCs on the placenta of livestock are also discussed, together with the molecular mechanism of EDCs acting in trophoblast cells. We describe how EDCs cross the membrane of trophoblasts to regulate signaling pathways, causing genetic and epigenetic changes that lead to changes in cell viability and invasiveness. Further studies on the effects of EDCs on placenta may draw attention to the correct use of products containing EDCs during pregnancy." {{placenta}}</div></td></tr>
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</table>Z8600021https://embryology.med.unsw.edu.au/embryology/index.php?title=Abnormal_Development_-_Chemicals&diff=383186&oldid=prevZ8600021 at 02:53, 16 Haziran 20192019-06-16T02:53:33Z<p></p>
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<td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">Revision as of 12:53, 16 Haziran 2019</td>
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<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>|</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>|</div></td></tr>
<tr><td class="diff-marker" data-marker="−"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div>* '''Review - A mechanism for the effect of endocrine disrupting chemicals on placentation'''{{#pmid:31132539|PMID31132539}} "Numerous recent studies have shown that endocrine disrupting chemicals (EDCs) in the body of pregnant women can pass through the placenta and be exposed to the fetus, leading to fetal development and cognitive impairment. Placentation through invasion of trophoblast cells and vascular remodeling is essential to maintaining maternal and fetal health throughout the pregnancy. Abnormal placentation can lead to pregnancy disorders such as preeclampsia (PE) and intrauterine growth retardation (IUGR). However, many studies have not been conducted on whether EDCs can inhibit the development and function of the placenta. Isolating placental tissues to analyze the effect of EDCs on placentation has several limitations. In this review, we discussed the types of EDCs that can pass through the placental barrier and accumulate in the placenta with relative outcome. EDCs can be released from a variety of products including plasticizers, pesticides, and retardant. We also discussed the development and dysfunction of the placenta when EDCs were treated on trophoblast cells or pregnant rodent models. The effects of EDCs on the placenta of livestock are also discussed, together with the molecular mechanism of EDCs acting in trophoblast cells. We describe how EDCs cross the membrane of trophoblasts to regulate signaling pathways, causing genetic and epigenetic changes that lead to changes in cell viability and invasiveness. Further studies on the effects of EDCs on placenta may draw attention to the correct use of products containing EDCs during pregnancy."</div></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div>* '''Review - A mechanism for the effect of endocrine disrupting chemicals on placentation'''{{#pmid:31132539|PMID31132539}} "Numerous recent studies have shown that endocrine disrupting chemicals (EDCs) in the body of pregnant women can pass through the placenta and be exposed to the fetus, leading to fetal development and cognitive impairment. Placentation through invasion of trophoblast cells and vascular remodeling is essential to maintaining maternal and fetal health throughout the pregnancy. Abnormal placentation can lead to pregnancy disorders such as preeclampsia (PE) and intrauterine growth retardation (IUGR). However, many studies have not been conducted on whether EDCs can inhibit the development and function of the placenta. Isolating placental tissues to analyze the effect of EDCs on placentation has several limitations. In this review, we discussed the types of EDCs that can pass through the placental barrier and accumulate in the placenta with relative outcome. EDCs can be released from a variety of products including plasticizers, pesticides, and retardant. We also discussed the development and dysfunction of the placenta when EDCs were treated on trophoblast cells or pregnant rodent models. The effects of EDCs on the placenta of livestock are also discussed, together with the molecular mechanism of EDCs acting in trophoblast cells. We describe how EDCs cross the membrane of trophoblasts to regulate signaling pathways, causing genetic and epigenetic changes that lead to changes in cell viability and invasiveness. Further studies on the effects of EDCs on placenta may draw attention to the correct use of products containing EDCs during pregnancy." <ins style="font-weight: bold; text-decoration: none;">{{placenta}}</ins></div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>* '''Toxicokinetics of bisphenol A, bisphenol S, and bisphenol F in a pregnancy {{sheep}} model'''{{#pmid:30583211|PMID30583211}} "Bisphenol A (BPA), S (BPS), and F (BPF) are among the most abundant bisphenols detected in humans, yet pregnancy toxicokinetics for BPS or BPF remain unknown. Because gestational BPS can disrupt placental function and result in reproductive and metabolic disorders in the progeny, the aim of the study was to investigate BPS and BPF toxicokinetics during pregnancy using an in vivo approach. Fetal catheterizations were conducted in pregnant sheep (n = 6) at mid-pregnancy and injected with either a single dose of BPS (n = 3, 0.5 mg/kg, s.c.), or a combination of BPS, BPF, and BPA (n = 3, 0.5 mg/kg for each chemical, s.c.). Maternal and fetal blood and urine and amniotic fluid were collected over 72 h and analyzed for bisphenols by HPLC-MS/MS. We observed significant differences in half-life, maximum concentration, and total body clearance in maternal circulation among bisphenols. Longer half-lives were observed in fetal vs. maternal circulation for all bisphenols. Fetal toxicokinetics differed among bisphenols with BPS having the longest fetal half-life. All bisphenols reached basal levels at 48 h in maternal plasma, but were still detectable in amniotic fluid, fetal urine, and fetal plasma at 72 h. In this first pregnancy toxicokinetic study of BPS and BPF we have demonstrated maternal and fetal toxicokinetic differences among all three bisphenols. Higher BPS persistence in the fetal compartment warrants studies into progeny adverse outcomes following gestational exposure. Additionally, toxicokinetic differences among bisphenols call for a more careful approach when extrapolating kinetic information from one bisphenol chemical to another."</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>* '''Toxicokinetics of bisphenol A, bisphenol S, and bisphenol F in a pregnancy {{sheep}} model'''{{#pmid:30583211|PMID30583211}} "Bisphenol A (BPA), S (BPS), and F (BPF) are among the most abundant bisphenols detected in humans, yet pregnancy toxicokinetics for BPS or BPF remain unknown. Because gestational BPS can disrupt placental function and result in reproductive and metabolic disorders in the progeny, the aim of the study was to investigate BPS and BPF toxicokinetics during pregnancy using an in vivo approach. Fetal catheterizations were conducted in pregnant sheep (n = 6) at mid-pregnancy and injected with either a single dose of BPS (n = 3, 0.5 mg/kg, s.c.), or a combination of BPS, BPF, and BPA (n = 3, 0.5 mg/kg for each chemical, s.c.). Maternal and fetal blood and urine and amniotic fluid were collected over 72 h and analyzed for bisphenols by HPLC-MS/MS. We observed significant differences in half-life, maximum concentration, and total body clearance in maternal circulation among bisphenols. Longer half-lives were observed in fetal vs. maternal circulation for all bisphenols. Fetal toxicokinetics differed among bisphenols with BPS having the longest fetal half-life. All bisphenols reached basal levels at 48 h in maternal plasma, but were still detectable in amniotic fluid, fetal urine, and fetal plasma at 72 h. In this first pregnancy toxicokinetic study of BPS and BPF we have demonstrated maternal and fetal toxicokinetic differences among all three bisphenols. Higher BPS persistence in the fetal compartment warrants studies into progeny adverse outcomes following gestational exposure. Additionally, toxicokinetic differences among bisphenols call for a more careful approach when extrapolating kinetic information from one bisphenol chemical to another."</div></td></tr>
</table>Z8600021https://embryology.med.unsw.edu.au/embryology/index.php?title=Abnormal_Development_-_Chemicals&diff=383182&oldid=prevZ8600021 at 02:52, 16 Haziran 20192019-06-16T02:52:08Z<p></p>
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<td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">Revision as of 12:52, 16 Haziran 2019</td>
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<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>|</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>|</div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">* '''Review - A mechanism for the effect of endocrine disrupting chemicals on placentation'''{{#pmid:31132539|PMID31132539}} "Numerous recent studies have shown that endocrine disrupting chemicals (EDCs) in the body of pregnant women can pass through the placenta and be exposed to the fetus, leading to fetal development and cognitive impairment. Placentation through invasion of trophoblast cells and vascular remodeling is essential to maintaining maternal and fetal health throughout the pregnancy. Abnormal placentation can lead to pregnancy disorders such as preeclampsia (PE) and intrauterine growth retardation (IUGR). However, many studies have not been conducted on whether EDCs can inhibit the development and function of the placenta. Isolating placental tissues to analyze the effect of EDCs on placentation has several limitations. In this review, we discussed the types of EDCs that can pass through the placental barrier and accumulate in the placenta with relative outcome. EDCs can be released from a variety of products including plasticizers, pesticides, and retardant. We also discussed the development and dysfunction of the placenta when EDCs were treated on trophoblast cells or pregnant rodent models. The effects of EDCs on the placenta of livestock are also discussed, together with the molecular mechanism of EDCs acting in trophoblast cells. We describe how EDCs cross the membrane of trophoblasts to regulate signaling pathways, causing genetic and epigenetic changes that lead to changes in cell viability and invasiveness. Further studies on the effects of EDCs on placenta may draw attention to the correct use of products containing EDCs during pregnancy."</ins></div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;"></ins></div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>* '''Toxicokinetics of bisphenol A, bisphenol S, and bisphenol F in a pregnancy {{sheep}} model'''{{#pmid:30583211|PMID30583211}} "Bisphenol A (BPA), S (BPS), and F (BPF) are among the most abundant bisphenols detected in humans, yet pregnancy toxicokinetics for BPS or BPF remain unknown. Because gestational BPS can disrupt placental function and result in reproductive and metabolic disorders in the progeny, the aim of the study was to investigate BPS and BPF toxicokinetics during pregnancy using an in vivo approach. Fetal catheterizations were conducted in pregnant sheep (n = 6) at mid-pregnancy and injected with either a single dose of BPS (n = 3, 0.5 mg/kg, s.c.), or a combination of BPS, BPF, and BPA (n = 3, 0.5 mg/kg for each chemical, s.c.). Maternal and fetal blood and urine and amniotic fluid were collected over 72 h and analyzed for bisphenols by HPLC-MS/MS. We observed significant differences in half-life, maximum concentration, and total body clearance in maternal circulation among bisphenols. Longer half-lives were observed in fetal vs. maternal circulation for all bisphenols. Fetal toxicokinetics differed among bisphenols with BPS having the longest fetal half-life. All bisphenols reached basal levels at 48 h in maternal plasma, but were still detectable in amniotic fluid, fetal urine, and fetal plasma at 72 h. In this first pregnancy toxicokinetic study of BPS and BPF we have demonstrated maternal and fetal toxicokinetic differences among all three bisphenols. Higher BPS persistence in the fetal compartment warrants studies into progeny adverse outcomes following gestational exposure. Additionally, toxicokinetic differences among bisphenols call for a more careful approach when extrapolating kinetic information from one bisphenol chemical to another."</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>* '''Toxicokinetics of bisphenol A, bisphenol S, and bisphenol F in a pregnancy {{sheep}} model'''{{#pmid:30583211|PMID30583211}} "Bisphenol A (BPA), S (BPS), and F (BPF) are among the most abundant bisphenols detected in humans, yet pregnancy toxicokinetics for BPS or BPF remain unknown. Because gestational BPS can disrupt placental function and result in reproductive and metabolic disorders in the progeny, the aim of the study was to investigate BPS and BPF toxicokinetics during pregnancy using an in vivo approach. Fetal catheterizations were conducted in pregnant sheep (n = 6) at mid-pregnancy and injected with either a single dose of BPS (n = 3, 0.5 mg/kg, s.c.), or a combination of BPS, BPF, and BPA (n = 3, 0.5 mg/kg for each chemical, s.c.). Maternal and fetal blood and urine and amniotic fluid were collected over 72 h and analyzed for bisphenols by HPLC-MS/MS. We observed significant differences in half-life, maximum concentration, and total body clearance in maternal circulation among bisphenols. Longer half-lives were observed in fetal vs. maternal circulation for all bisphenols. Fetal toxicokinetics differed among bisphenols with BPS having the longest fetal half-life. All bisphenols reached basal levels at 48 h in maternal plasma, but were still detectable in amniotic fluid, fetal urine, and fetal plasma at 72 h. In this first pregnancy toxicokinetic study of BPS and BPF we have demonstrated maternal and fetal toxicokinetic differences among all three bisphenols. Higher BPS persistence in the fetal compartment warrants studies into progeny adverse outcomes following gestational exposure. Additionally, toxicokinetic differences among bisphenols call for a more careful approach when extrapolating kinetic information from one bisphenol chemical to another."</div></td></tr>
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</table>Z8600021https://embryology.med.unsw.edu.au/embryology/index.php?title=Abnormal_Development_-_Chemicals&diff=381632&oldid=prevZ8600021 at 01:31, 31 Mayıs 20192019-05-31T01:31:02Z<p></p>
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<td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">Revision as of 11:31, 31 Mayıs 2019</td>
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<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">* '''Toxicokinetics of bisphenol A, bisphenol S, and bisphenol F in a pregnancy {{sheep}} model'''{{#pmid:30583211|PMID30583211}} "Bisphenol A (BPA), S (BPS), and F (BPF) are among the most abundant bisphenols detected in humans, yet pregnancy toxicokinetics for BPS or BPF remain unknown. Because gestational BPS can disrupt placental function and result in reproductive and metabolic disorders in the progeny, the aim of the study was to investigate BPS and BPF toxicokinetics during pregnancy using an in vivo approach. Fetal catheterizations were conducted in pregnant sheep (n = 6) at mid-pregnancy and injected with either a single dose of BPS (n = 3, 0.5 mg/kg, s.c.), or a combination of BPS, BPF, and BPA (n = 3, 0.5 mg/kg for each chemical, s.c.). Maternal and fetal blood and urine and amniotic fluid were collected over 72 h and analyzed for bisphenols by HPLC-MS/MS. We observed significant differences in half-life, maximum concentration, and total body clearance in maternal circulation among bisphenols. Longer half-lives were observed in fetal vs. maternal circulation for all bisphenols. Fetal toxicokinetics differed among bisphenols with BPS having the longest fetal half-life. All bisphenols reached basal levels at 48 h in maternal plasma, but were still detectable in amniotic fluid, fetal urine, and fetal plasma at 72 h. In this first pregnancy toxicokinetic study of BPS and BPF we have demonstrated maternal and fetal toxicokinetic differences among all three bisphenols. Higher BPS persistence in the fetal compartment warrants studies into progeny adverse outcomes following gestational exposure. Additionally, toxicokinetic differences among bisphenols call for a more careful approach when extrapolating kinetic information from one bisphenol chemical to another."</ins></div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;"></ins></div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>* '''Endocrine Disrupting Chemicals: An Occult Mediator of Metabolic Disease'''{{#pmid:30881345|PMID30881345}} "Endocrine disrupting chemicals (EDCs), a heterogeneous group of exogenous chemicals that can interfere with any aspect of endogenous hormones, represent an emerging global threat for human metabolism. There is now considerable evidence that the observed upsurge of metabolic disease cannot be fully attributed to increased caloric intake, physical inactivity, sleep deficit, and ageing. Among environmental factors implicated in the global deterioration of metabolic health, EDCs have drawn the biggest attention of scientific community, and not unjustifiably. EDCs unleash a coordinated attack toward multiple components of human metabolism, including crucial, metabolically-active organs such as hypothalamus, adipose tissue, pancreatic beta cells, skeletal muscle, and liver. Specifically, EDCs' impact during critical developmental windows can promote the disruption of individual or multiple systems involved in metabolism, via inducing epigenetic changes that can permanently alter the epigenome in the germline, enabling changes to be transmitted to the subsequent generations. The clear effect of this multifaceted attack is the manifestation of metabolic disease, clinically expressed as obesity, metabolic syndrome, diabetes mellitus, and non-alcoholic fatty liver disease."</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>* '''Endocrine Disrupting Chemicals: An Occult Mediator of Metabolic Disease'''{{#pmid:30881345|PMID30881345}} "Endocrine disrupting chemicals (EDCs), a heterogeneous group of exogenous chemicals that can interfere with any aspect of endogenous hormones, represent an emerging global threat for human metabolism. There is now considerable evidence that the observed upsurge of metabolic disease cannot be fully attributed to increased caloric intake, physical inactivity, sleep deficit, and ageing. Among environmental factors implicated in the global deterioration of metabolic health, EDCs have drawn the biggest attention of scientific community, and not unjustifiably. EDCs unleash a coordinated attack toward multiple components of human metabolism, including crucial, metabolically-active organs such as hypothalamus, adipose tissue, pancreatic beta cells, skeletal muscle, and liver. Specifically, EDCs' impact during critical developmental windows can promote the disruption of individual or multiple systems involved in metabolism, via inducing epigenetic changes that can permanently alter the epigenome in the germline, enabling changes to be transmitted to the subsequent generations. The clear effect of this multifaceted attack is the manifestation of metabolic disease, clinically expressed as obesity, metabolic syndrome, diabetes mellitus, and non-alcoholic fatty liver disease."</div></td></tr>
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</table>Z8600021https://embryology.med.unsw.edu.au/embryology/index.php?title=Abnormal_Development_-_Chemicals&diff=380956&oldid=prevZ8600021 at 06:35, 20 Mayıs 20192019-05-20T06:35:54Z<p></p>
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<td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">Revision as of 16:35, 20 Mayıs 2019</td>
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<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><br/></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>* '''Genotoxic and mutagenic studies of teratogens in developing {{rat}} and {{mouse}}'''{{#pmid:29745766|PMID29745766}} "In this review, genotoxic and mutagenic effects of teratogenic chemical agents in both rat and mouse have been reviewed. Of these chemicals, 97 are drugs and 33 are pesticides or belong to other groups. Large literature searches were conducted to determine the effects of chemicals on chromosome abnormalities, sister chromatid exchanges, and micronucleus formation in experimental animals such as rats and mice. In addition, studies that include unscheduled DNA synthesis, DNA adduct formations, and gene mutations, which help to determine the genotoxicity or mutagenicity of chemicals, have been reviewed. It has been estimated that 46.87% of teratogenic drugs and 48.48% of teratogenic pesticides are positive in all tests. So, all of the teratogens involved in this group have genotoxic and mutagenic effects. On the other hand, 36.45% of the drugs and 21.21% of the pesticides have been found to give negative results in at least one test, with the majority of the tests giving positive results. However, only 4.16% of the drugs and 18.18% of the pesticides were determined to give negative results in the majority of the tests. Among tests with major negative results, 12.50% of the teratogenic drugs and 12.12% of the teratogenic pesticides were negative in all conducted tests."</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>* '''Genotoxic and mutagenic studies of teratogens in developing {{rat}} and {{mouse}}'''{{#pmid:29745766|PMID29745766}} "In this review, genotoxic and mutagenic effects of teratogenic chemical agents in both rat and mouse have been reviewed. Of these chemicals, 97 are drugs and 33 are pesticides or belong to other groups. Large literature searches were conducted to determine the effects of chemicals on chromosome abnormalities, sister chromatid exchanges, and micronucleus formation in experimental animals such as rats and mice. In addition, studies that include unscheduled DNA synthesis, DNA adduct formations, and gene mutations, which help to determine the genotoxicity or mutagenicity of chemicals, have been reviewed. It has been estimated that 46.87% of teratogenic drugs and 48.48% of teratogenic pesticides are positive in all tests. So, all of the teratogens involved in this group have genotoxic and mutagenic effects. On the other hand, 36.45% of the drugs and 21.21% of the pesticides have been found to give negative results in at least one test, with the majority of the tests giving positive results. However, only 4.16% of the drugs and 18.18% of the pesticides were determined to give negative results in the majority of the tests. Among tests with major negative results, 12.50% of the teratogenic drugs and 12.12% of the teratogenic pesticides were negative in all conducted tests."</div></td></tr>
<tr><td class="diff-marker" data-marker="−"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div><del style="font-weight: bold; text-decoration: none;"></del></div></td><td colspan="2" class="diff-side-added"></td></tr>
<tr><td class="diff-marker" data-marker="−"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #ffe49c; vertical-align: top; white-space: pre-wrap;"><div><del style="font-weight: bold; text-decoration: none;">* '''Effects of environmental Bisphenol A exposures on germ cell development and {{Leydig cells}} function in the human fetal''' testis{{#pmid:29385186|PMID29385186}} "Using an organotypic culture system termed human Fetal Testis Assay (hFeTA) we previously showed that 0.01 μM BPA decreases basal, but not LH-stimulated, testosterone secreted by the first trimester human fetal testis. The present study was conducted to determine the potential for a long-term antiandrogenic effect of BPA using a xenograft model, and also to study the effect of BPA on germ cell development using both the hFETA and xenograft models. ... Exposure to BPA at environmentally relevant concentrations impairs germ cell development in first trimester human fetal testis, whilst gonadotrophin-stimulated testosterone production was unaffected in both first and second trimester testis. Studies using first trimester human fetal testis demonstrate the complementarity of the FeTA and xenograft models for determining the respective short-term and long term effects of environmental exposures."</del></div></td><td colspan="2" class="diff-side-added"></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>|}</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>|}</div></td></tr>
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<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;">* '''Effects of environmental Bisphenol A exposures on germ cell development and {{Leydig cells}} function in the human fetal''' testis{{#pmid:29385186|PMID29385186}} "Using an organotypic culture system termed human Fetal Testis Assay (hFeTA) we previously showed that 0.01 μM BPA decreases basal, but not LH-stimulated, testosterone secreted by the first trimester human fetal testis. The present study was conducted to determine the potential for a long-term antiandrogenic effect of BPA using a xenograft model, and also to study the effect of BPA on germ cell development using both the hFETA and xenograft models. ... Exposure to BPA at environmentally relevant concentrations impairs germ cell development in first trimester human fetal testis, whilst gonadotrophin-stimulated testosterone production was unaffected in both first and second trimester testis. Studies using first trimester human fetal testis demonstrate the complementarity of the FeTA and xenograft models for determining the respective short-term and long term effects of environmental exposures."</ins></div></td></tr>
<tr><td colspan="2" class="diff-side-deleted"></td><td class="diff-marker" data-marker="+"></td><td style="color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #a3d3ff; vertical-align: top; white-space: pre-wrap;"><div><ins style="font-weight: bold; text-decoration: none;"></ins></div></td></tr>
<tr><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>* '''Low-dose exposure to bisphenol A (BPA) and replacement bisphenol S induces precocious hypothalamic neurogenesis in embryonic zebrafish'''{{#pmid:25583509|PMID25583509}} "Here, we used zebrafish to link BPA mechanistically to disease etiology. Strikingly, treatment of embryonic zebrafish with very low-dose BPA (0.0068 μM, 1,000-fold lower than the accepted human daily exposure) and bisphenol S (BPS), a common analog used in BPA-free products, resulted in 180% and 240% increases, respectively, in neuronal birth (neurogenesis) within the hypothalamus, a highly conserved brain region involved in hyperactivity. Furthermore, restricted BPA/BPS exposure specifically during the neurogenic window caused later hyperactive behaviors in zebrafish larvae. Unexpectedly, we show that BPA-mediated precocious neurogenesis and the concomitant behavioral phenotype were not dependent on predicted estrogen receptors but relied on androgen receptor-mediated up-regulation of aromatase. Although human epidemiological results are still emerging, an association between high maternal urinary BPA during gestation and hyperactivity and other behavioral disturbances in the child has been suggested. Our studies here provide mechanistic support that the neurogenic period indeed may be a window of vulnerability and uncovers previously unexplored avenues of research into how endocrine disruptors might perturb early brain development. Furthermore, our results show that BPA-free products are not necessarily safer and support the removal of all bisphenols from consumer merchandise." {{zebrafish}}</div></td><td class="diff-marker"></td><td style="background-color: #f8f9fa; color: #202122; font-size: 88%; border-style: solid; border-width: 1px 1px 1px 4px; border-radius: 0.33em; border-color: #eaecf0; vertical-align: top; white-space: pre-wrap;"><div>* '''Low-dose exposure to bisphenol A (BPA) and replacement bisphenol S induces precocious hypothalamic neurogenesis in embryonic zebrafish'''{{#pmid:25583509|PMID25583509}} "Here, we used zebrafish to link BPA mechanistically to disease etiology. Strikingly, treatment of embryonic zebrafish with very low-dose BPA (0.0068 μM, 1,000-fold lower than the accepted human daily exposure) and bisphenol S (BPS), a common analog used in BPA-free products, resulted in 180% and 240% increases, respectively, in neuronal birth (neurogenesis) within the hypothalamus, a highly conserved brain region involved in hyperactivity. Furthermore, restricted BPA/BPS exposure specifically during the neurogenic window caused later hyperactive behaviors in zebrafish larvae. Unexpectedly, we show that BPA-mediated precocious neurogenesis and the concomitant behavioral phenotype were not dependent on predicted estrogen receptors but relied on androgen receptor-mediated up-regulation of aromatase. Although human epidemiological results are still emerging, an association between high maternal urinary BPA during gestation and hyperactivity and other behavioral disturbances in the child has been suggested. Our studies here provide mechanistic support that the neurogenic period indeed may be a window of vulnerability and uncovers previously unexplored avenues of research into how endocrine disruptors might perturb early brain development. Furthermore, our results show that BPA-free products are not necessarily safer and support the removal of all bisphenols from consumer merchandise." {{zebrafish}}</div></td></tr>
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</table>Z8600021https://embryology.med.unsw.edu.au/embryology/index.php?title=Abnormal_Development_-_Chemicals&diff=380950&oldid=prevZ8600021 at 06:34, 20 Mayıs 20192019-05-20T06:34:26Z<p></p>
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<td colspan="2" style="background-color: #fff; color: #202122; text-align: center;">Revision as of 16:34, 20 Mayıs 2019</td>
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