Talk:Abnormal Development - Heavy Metals

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On this website the Discussion Tab or "talk pages" for a topic has been used for several purposes: References - recent and historic that relates to the topic Additional topic information - currently prepared in draft format Links - to related webpages Topic page - an edit history as used on other Wiki sites Lecture/Practical - student feedback Student Projects - online project discussions. Links: Pubmed Most Recent | Reference Tutorial | Journal Searches Glossary Links Glossary: A | B | C | D | E | F | G | H | I | J | K | L | M | N | O | P | Q | R | S | T | U | V | W | X | Y | Z | Numbers | Symbols | Term Link Cite this page: Hill, M.A. (2024, April 20) Embryology Abnormal Development - Heavy Metals. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Talk:Abnormal_Development_-_Heavy_Metals

2001

Interrelations of lead levels in bone, venous blood, and umbilical cord blood with exogenous lead exposure through maternal plasma lead in peripartum women

Environ Health Perspect. 2001 May;109(5):527-32.

Chuang HY, Schwartz J, Gonzales-Cossio T, Lugo MC, Palazuelos E, Aro A, Hu H, Hernandez-Avila M. Source Department of Environmental Health, Harvard School of Public Health, Boston, Massachusetts, USA. Abstract Recent research has raised the possibility that fetal lead exposure is not estimated adequately by measuring lead content in maternal whole blood lead because of the variable partitioning of lead in whole blood between plasma and red blood cells. Lead in maternal plasma may derive in large part from maternal bone lead stores. In this study we aimed to estimate the contribution of maternal whole blood lead, maternal bone lead levels, and environmental lead to umbilical cord blood lead levels (as a measure of fetal lead exposure). In the model, we assumed that lead from all of these sources reaches the fetus through the maternal plasma lead pathway. In 1994-1995, we recruited 615 pregnant women for a study of lead exposure and reproductive outcomes in Mexico City. We gathered maternal and umbilical cord blood samples within 12 hr of each infant's delivery and measured maternal lead levels in cortical bone and trabecular bone by a K-X-ray fluorescence (K-XRF) instrument within 1 month after delivery. We administered a questionnaire to assess use of lead-glazed ceramics (LGC) to cook food and we obtained data on regional air lead levels during the 2 months before delivery. We used structural equation models (SEMs) to estimate plasma lead as the unmeasured (latent) variable and to quantify the interrelations of plasma lead, the other lead biomarkers, and environmental lead exposure. In the SEM analysis, a model that allowed plasma lead to vary freely from whole blood lead explained the variance of cord blood lead (as reflected by a total model R(2); R(2) = 0.79) better than did a model without plasma lead (r(2) = 0.67). Cortical bone lead, trabecular bone lead, use of LGC, and mean air lead level contributed significantly to plasma lead. The exchange of lead between plasma and red blood cells was mostly in the direction of plasma to cells. According to the final model, an increase in trabecular bone lead and cortical bone lead was associated with increases in cord blood lead of 0.65 and 0.25 microg/dL, respectively. An increase of 0.1 microg/m(3) in air lead was associated with an increase in the mean level of fetal cord blood lead by 0.67 microg/dL. With one additional day of LCG use per week in the peripartum period, the mean fetal blood lead level increased by 0.27 microg/dL. Our analyses suggested that maternal plasma lead varies independently from maternal whole blood lead and that the greatest influences on maternal plasma lead are maternal bone lead stores, air lead exposures, and recent cooking with LGC. The contributions from endogenous (bone) and exogenous (environmental) sources were relatively equal. Measurement of plasma and bone lead may be important in accurately assessing fetal lead exposure and its major sources, particularly if exogenous exposures decline.

PMID: 11401766

chromium

Chromium III histidinate exposure modulates gene expression in HaCaT human keratinocytes exposed to oxidative stress

Hazane-Puch F, Benaraba R, Valenti K, Osman M, Laporte F, Favier A, Anderson RA, Roussel AM, Hininger-Favier I. Biol Trace Elem Res. 2010 Oct;137(1):23-39. Epub 2009 Nov 10. PMID: 19902159

Chromium effects on free radical processes in goldfish tissues: comparison of Cr(III) and Cr(VI) exposures on oxidative stress markers, glutathione status and antioxidant enzymes

Kubrak OI, Lushchak OV, Lushchak JV, Torous IM, Storey JM, Storey KB, Lushchak VI. Comp Biochem Physiol C Toxicol Pharmacol. 2010 Sep;152(3):360-70. Epub 2010 Jun 12. PMID: 20547245

Lactational hexavalent chromium exposure-induced oxidative stress in rat uterus is associated with delayed puberty and impaired gonadotropin levels

Samuel JB, Stanley JA, Roopha DP, Vengatesh G, Anbalagan J, Banu SK, Aruldhas MM. Hum Exp Toxicol. 2010 Mar 4. [Epub ahead of print] PMID: 20203132

Reproductive toxicity of chromium in adult bonnet monkeys (Macaca radiata Geoffrey). Reversible oxidative stress in the semen

Subramanian S, Rajendiran G, Sekhar P, Gowri C, Govindarajulu P, Aruldhas MM. Toxicol Appl Pharmacol. 2006 Sep 15;215(3):237-49. Epub 2006 May 6. PMID: 16678873

iron

Maternal iron status influences iron transfer to the fetus during the third trimester of pregnancy.

Am J Clin Nutr. 2003 Apr;77(4):924-30. O'Brien KO, Zavaleta N, Abrams SA, Caulfield LE.

Johns Hopkins Bloomberg School of Public Health, Baltimore, MD 21205-2179, USA. kobrien@jhsph.edu Abstract BACKGROUND: The effect of maternal iron status on fetal iron deposition is uncertain. OBJECTIVE: We used a unique stable-isotope technique to assess iron transfer to the fetus in relation to maternal iron status. DESIGN: The study group comprised 41 Peruvian women. Of these women, 26 received daily prenatal supplements containing iron and folate (n = 11; Fe group) or iron, folate, and zinc (n = 15; Fe+Zn group) from week 10-24 of pregnancy to 1 mo postpartum. The remaining 15 women (control group) received iron supplementation only during the final month of pregnancy. During the third trimester of pregnancy (+/- SD: 32.9 +/- 1.4 wk gestation) oral 57Fe (10 mg) and intravenous 58Fe (0.6 mg) stable iron isotopes were administered to the women, and isotope enrichment and iron-status indicators were measured in cord blood at delivery. RESULTS: The net amount of 57Fe in the neonates' circulation (from maternal oral dosing) was significantly related to maternal iron absorption (P < 0.005) and inversely related to maternal iron status during the third trimester of pregnancy: serum ferritin (P < 0.0001), serum folate (P < 0.005), and serum transferrin receptors (P < 0.02). Significantly more 57Fe was transferred to the neonates in non-iron-supplemented women: 0.112 +/- 0.031 compared with 0.078 +/- 0.042 mg in the control group (n = 15) and the Fe and Fe+Zn groups (n = 24), respectively (P < 0.01). In contrast, 58Fe tracer in the neonates' circulation was not significantly related to maternal iron status. CONCLUSION: The transfer of dietary iron to the fetus is regulated in response to maternal iron status at the level of the gut.

PMID: 12663293

mercury

Tohoku J Exp Med. 2003 Sep;201(1):1-9. Behavioral teratology of mercury and its compounds. Satoh H.

Environmental Health Sciences, Tohoku University Graduate School of Medicine, Sendai 980-8575, Japan. h.satoh@ehs.med.tohoku.ac.jp Abstract Mercury and its compounds have a wide spectrum of toxicities depending upon the chemical forms and modes of exposure. Among the various chemical forms, mercury vapor and methylmercury are well known and established as neurotoxic agents. Since the disasters in Minamata and Iraq, in which fetuses were more susceptible than adults to methylmercury exposure, much attention has been focused on prenatal exposure to mercury and its consequence. Recently postnatal effects of in utero exposure to methylmercury through fish (and marine mammals) consumption by mothers have been concerned and several epidemiological studies have been conducted. Therefore, one of the most seriously concerned issues is the postnatal effects of in utero exposure to methylmercury. Because of these observations in humans, animal experiments have been conducted employing prenatal exposure to low levels of mercury. This paper reviews the animal (rodents) experiments concerning "behavioral teratology" of mercury for better understanding of effects of prenatal exposure to mercury and its compounds in addition to commentary on history and framework of behavioral teratology.

PMID: 14609255

For chemical page - formaldehyde

Embryo toxicity and teratogenicity of formaldehyde

Thrasher JD, Kilburn KH. Arch Environ Health. 2001 Jul-Aug;56(4):300-11. Review. PMID: 11572272

"C-14 formaldehyde crosses the placenta and enters fetal tissues. The incorporated radioactivity is higher in fetal organs (i.e., brain and liver) than in maternal tissues. The incorporation mechanism has not been studied fully, but formaldehyde enters the single-carbon cycle and is incorporated as a methyl group into nucleic acids and proteins. Also, formaldehyde reacts chemically with organic compounds (e.g., deoxyribonucleic acid, nucleosides, nucleotides, proteins, amino acids) by addition and condensation reactions, thus forming adducts and deoxyribonucleic acid-protein crosslinks. "