In vivo evaluation of teratogenesis and cytogenetic changes following methylmercuric chloride treatment

Curle, D C; Ray, M.; Persaud, T. V. N.

doi:10.1002/ar.1092190309

Cited by 16 publications

(6 citation statements)

References 37 publications

(44 reference statements)

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“…Mammalian and invertebrate studies indicate that exposure to MeHg can cause delays in animal development and confer embryonic defects (Carvalho et al, 2008;Curle et al, 1987;Weis, 2009). In order to determine if MeHg can affect normal development, we examined the rate of development of animals grown on a low concentration of MeHg from L1 to the L4 stage.…”

Section: Mehg Confers Developmental Delays and Embryonic Defectsmentioning

confidence: 99%

SKN-1/Nrf2 Inhibits Dopamine Neuron Degeneration in a Caenorhabditis elegans Model of Methylmercury Toxicity

VanDuyn

Settivari

Wong

et al. 2010

Toxicological Sciences

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Methylmercury (MeHg) exposure from occupational, environmental, and food sources is a significant threat to public health. MeHg poisonings in adults may result in severe psychological and neurological deficits, and in utero exposures can confer embryonic defects and developmental delays. Recent epidemiological and vertebrate studies suggest that MeHg exposure may also contribute to dopamine (DA) neuron vulnerability and the propensity to develop Parkinson's disease (PD). In this study, we describe a Caenorhabditis elegans model of MeHg toxicity that shows that low, chronic exposure confers embryonic defects, developmental delays, decreases in brood size and animal viability, and DA neuron degeneration. Toxicant exposure results in the robust induction of the glutathione-S-transferases (GSTs) gst-4 and gst-38 that are largely dependent on the PD-associated phase II antioxidant transcription factor SKN-1/Nrf2. We also demonstrate that the expression of SKN-1, a protein previously localized to a small subset of chemosensory neurons and intestinal cells in the nematode, is also expressed in the DA neurons, and a reduction in SKN-1 gene expression increases MeHg-induced animal vulnerability and DA neuron degeneration. These studies recapitulate fundamental hallmarks of MeHg-induced mammalian toxicity, identify a key molecular regulator of toxicant-associated whole-animal and DA neuron vulnerability, and suggest that the nematode will be a useful in vivo tool to identify and characterize mediators of MeHg-induced developmental and DA neuron pathologies.

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Section: Mehg Confers Developmental Delays and Embryonic Defectsmentioning

confidence: 99%

SKN-1/Nrf2 Inhibits Dopamine Neuron Degeneration in a Caenorhabditis elegans Model of Methylmercury Toxicity

VanDuyn

Settivari

Wong

et al. 2010

Toxicological Sciences

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“…Hg toxicity is associated with superoxide radical generation and GSH reduction. 43 HgCl 2 is also known to increase the production of many reactive oxygen species, such as O Á 2 À and H 2 O 2 and subsequently oxidative tissue damage. 5,44,45 The protective effects of garlic have been attributed to the presence of organosulphur compounds like diallyl sulphide (DAS), diallyl disulphide, ajoene, allixin, allyl mercaptans and allyl methyl sulphides.…”

Section: Discussionmentioning

confidence: 99%

“…Hg toxicity is associated with superoxide radical generation and GSH reduction. 43 HgCl 2 is also known to increase the production of many reactive oxygen species, such as O 2 − · and H 2 O 2 and subsequently oxidative tissue damage. 5,44,45…”

Section: Discussionmentioning

confidence: 99%

Protective effect of diallylsulphide against mercuric chloride-induced hepatic injury in rats

Ansar

Iqbal

2016

Hum Exp Toxicol

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The present study was undertaken to evaluate the effect of diallylsulphide (DAS) against mercuric chloride (HgCl2)-induced oxidative stress in rat livers. Rats were randomly divided into four groups of six rats each and exposed to HgCl2 (50 mg/kg/body weight (b.w.)) intraperitoneally and/or DAS (200 mg/kg/b.w.) by gavage. HgCl2 administration enhanced alanine aminotransferase (AST) and aspartate aminotransferase (ALT) levels ( p < 0.05) with reduction in the levels of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px). However, treatment with DAS markedly attenuated HgCl2-induced biochemical alterations in liver and serum transaminases (AST and ALT; p < 0.05). Further, biochemical results were confirmed by histopathological changes as compared to HgCl2-intoxicated rats. Histopathology of liver also showed that administration of DAS significantly reduced the damage generated by HgCl2. The present study suggests that DAS shows antioxidant activity and plays a protective role against mercury-induced oxidative damage in the rat livers.

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“…S, Splanchnopleuric extraembryonic mesoderm. (Spyker and Smithberg, 1972;Harris et al, 1972;Inouye and Murakami, 1975;Su and Okita, 1976;Kajiwara and Inouye, 1986;Curle et al, 1987). Derangement of the cerebral cortical plate and dilatation of the lateral ventricles are produced in the brain of fetal mice and rats by maternal treatment with methylmercury (Inouye and Murakami, 1975).…”

Section: Orgaaic Mercurymentioning

confidence: 99%

Teratology of Heavy Metals: Mercury and Other Contaminants*

Inouye

1989

Congenital Anomalies

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Modern industrialization has introduced harmful metals into our environment, and there has been a good deal of speculation that heavy metals can cause teratogenesis. In fact many metals have been confirmed to have em‐bryotoxicity in experimental animals, but only a few elements (e.g., mercury, lead, etc.) are known to be human teratogens. Liquid metallic mercury is hardly absorbed from the gastrointestinal tract. Inorganic mercury is also poorly absorbed, i.e., around 2% of ingested mercuric chloride is absorbed. Uptake of inorganic mercury by the fetus is very low. An experiment using mice revealed that a significant proportion of mercury is blocked in the yolk sack. Among the organic mercury compounds, the most accumulated knowledge pertains to methylmercury compounds. Methyl‐mercury is efficiently absorbed through the intestinal tract and skin. It crosses the human placenta with infantile blood levels in excess of the mother's blood, giving rise to a higher risk for the fetus. Pathological features of children's brains affected by prenatal methylmercury exposure are the outcome of disturbances in the development of the brain; microcephaly, dilated lateral ventricles, as well as derangement in the fundamental structuring of gray matter as the result of abnormal neuronal migration. Degeneration of already formed nerve cells is involved in some cases. Lead has been shown to pass through the human placenta readily, and the concentration in the umbilical cord blood is 80‐90 % as high as that in the maternal blood. A large cohort study suggests that increased exposure to lead from the environment in the prenatal and early postnatal periods results in the deficit of mental development. Teratogenicity of many metal compounds such as aluminum, cadmium, chromium, indium, nickel, platinum, tellurium, thallium, ytterbium and zinc salts has been confirmed in experimental animals. Some metalloids (e.g., arsenic, selenium and lithium) appear to have teratogenic potential for humans.

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In vivo evaluation of teratogenesis and cytogenetic changes following methylmercuric chloride treatment

Cited by 16 publications

References 37 publications

SKN-1/Nrf2 Inhibits Dopamine Neuron Degeneration in a Caenorhabditis elegans Model of Methylmercury Toxicity

SKN-1/Nrf2 Inhibits Dopamine Neuron Degeneration in a Caenorhabditis elegans Model of Methylmercury Toxicity

Protective effect of diallylsulphide against mercuric chloride-induced hepatic injury in rats

Teratology of Heavy Metals: Mercury and Other Contaminants*

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