&lt;i&gt;S&lt;/i&gt;-Mercuration of cellular proteins by methylmercury and its toxicological implications

Kanda, Hironori; Shinkai, Yasuhiro; Kumagai, Yoshito

doi:10.2131/jts.39.687

Cited by 47 publications

(32 citation statements)

References 126 publications

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“…Mitochondrial thiol status and antioxidant levels were found to be significantly declined due to MeHg exposure which could be due to the covalent binding of MeHg to reactive thiols of cellular proteins. MeHg exposure induced reduction in antioxidant levels has been reported in earlier studies (Farina et al, 2011; Kanda et al, 2014). Out of the four doses studied, 30 mg/kg b.w.…”

Section: Discussionsupporting

confidence: 73%

Fisetin impedes developmental methylmercury neurotoxicity via downregulating apoptotic signalling pathway and upregulating Rho GTPase signalling pathway in hippocampus of F₁ generation rats

Jacob

Sumathi

2018

Intl J of Devlp Neuroscience

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Methyl mercury is a teratogenic and neurodevelopmental toxicant in the environment. MeHg affects several biological pathways critical for brain development. The present study validated the effect of Fisetin on developmental MeHg exposure induced alterations in mitochondrial apoptotic pathway and Rho GTPase mRNA expressions in hippocampus of F generation rats. Pregnant Wistar rats were grouped as Group I : administered with vehicle control, Group II: MeHg (1.5 mg/kg b.w), Group III: MeHg + Fisetin (10 mg/kg b.w), Group IV: MeHg + Fisetin (30 mg/kg b.w), Group V: MeHg + Fisetin (50 mg/kg b.w), Group VI: MeHg + Fisetin (70 mg/kg b.w), Group VII: Fisetin (30 mg/kg b.w) alone. Fisetin reduced mercury accumulation in offspring brain. In hippocampus, Fisetin preserved mitochondrial total thiol status, glutathione antioxidant system, mitochondrial metabolic integrity and respiratory chain activity. Fisetin ameliorated apoptotic signals by preventing Cytochrome c release, down regulating ERK 1/2 and Caspase 3 gene expression. Fisetin also upregulated mRNA expressions of RhoA/Rac1/Cdc42 in hippocampus. Predominant effect of Fisetin was to reduce mercury accumulation in offspring brain there by diminishing the toxic effect of MeHg. Hence we showed that, gestational intake of Fisetin (30 mg/kg b.w.) impedes developmental MeHg neurotoxicity by regulating mitochondrial apoptotic and Rho GTPase signalling molecules and by reducing the mercury accumulation in hippocampus of F generation rats.

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Section: Discussionsupporting

confidence: 73%

Fisetin impedes developmental methylmercury neurotoxicity via downregulating apoptotic signalling pathway and upregulating Rho GTPase signalling pathway in hippocampus of F₁ generation rats

Jacob

Sumathi

2018

Intl J of Devlp Neuroscience

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“…Methyl mercury (MeHg) is one of the most toxic species of Hg which is assimilated into the water and food, and biomagnifies upwards in food chains 4 . MeHg can induce changes in mitochondria dyshomeostasis, increase the generation of reactive oxygen species, disturb oxidative phosphorylation and electron transport 5, 6 which lead to lipid peroxidation and cell death 6–8 . It has long been observed that selenium (Se) protects organism from the toxicity of MeHg 9, 10 .…”

Section: Introductionmentioning

confidence: 99%

Selenocystine against methyl mercury cytotoxicity in HepG2 cells

Wang

Chen

et al. 2017

Sci Rep

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Methyl mercury (MeHg) is a highly toxic substance and the effect of selenium against MeHg toxicity is a hot topic. Until now, no related works have been reported from the view of the point of elemental speciation which is promising to study the mechanism at the molecular level. In this work, to reveal the effect of selenocystine (SeCys2) against MeHg cytotoxicity in HepG2 cells, a comprehensive analytical platform for speciation study of mercury and selenium in MeHg incubated or MeHg and SeCys2 co-incubated HepG2 cells was developed by integrating liquid chromatography (LC) - inductively coupled plasma mass spectrometry (ICP-MS) hyphenated techniques and chip-based pretreatment method. Interesting phenomenon was found that the co-incubation of MeHg with SeCys2 promoted the uptake of MeHg in HepG2 cells, but reduced the cytotoxicity of MeHg. Results obtained by ICP-MS based hyphenated techniques revealed a possible pathway for the incorporation and excretion of mercury species with the coexistence of SeCys2. The formation of MeHg and SeCys2 aggregation promotes the uptake of MeHg; majority of MeHg transforms into small molecular complexes (MeHg-glutathione (GSH) and MeHg-cysteine (Cys)) in HepG2 cells; and MeHg-GSH is the elimination species which results in reducing the cytotoxicity of MeHg.

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“…Methylmercury is an environmental pollutant known as the cause of Minamata disease, and severe central nervous system damage123. In sea- and fresh water, methylmercury bioaccumulates through the food chain to relatively high concentrations in the muscle of fish.…”

mentioning

confidence: 99%

Methylmercury induces the expression of TNF-α selectively in the brain of mice

Iwai-Shimada

Takahashi

Kim

et al. 2016

Sci Rep

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Methylmercury selectively damages the central nervous system (CNS). The tumor necrosis factor (TNF) superfamily includes representative cytokines that participate in the inflammatory response as well as cell survival, and apoptosis. In this study, we found that administration of methylmercury selectively induced TNF-α expression in the brain of mice. Although the accumulated mercury concentration in the liver and kidneys was greater than in the brain, TNF-α expression was induced to a greater extent in brain. Thus, it is possible that there may exist a selective mechanism by which methylmercury induces TNF-α expression in the brain. We also found that TNF-α expression was induced by methylmercury in C17.2 cells (mouse neural stem cells) and NF-κB may participate as a transcription factor in that induction. Further, we showed that the addition of TNF-α antagonist (WP9QY) reduced the toxicity of methylmercury to C17.2 cells. In contrast, the addition of recombinant TNF-α to the culture medium decreased the cell viability. We suggest that TNF-α may play a part in the selective damage of the CNS by methylmercury. Furthermore, our results indicate that the higher TNF-α expression induced by methylmercury maybe the cause of cell death, as TNF-α binds to its receptor after being released extracellularly.

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<i>S</i>-Mercuration of cellular proteins by methylmercury and its toxicological implications

Cited by 47 publications

References 126 publications

Fisetin impedes developmental methylmercury neurotoxicity via downregulating apoptotic signalling pathway and upregulating Rho GTPase signalling pathway in hippocampus of F₁ generation rats

Fisetin impedes developmental methylmercury neurotoxicity via downregulating apoptotic signalling pathway and upregulating Rho GTPase signalling pathway in hippocampus of F₁ generation rats

Selenocystine against methyl mercury cytotoxicity in HepG2 cells

Methylmercury induces the expression of TNF-α selectively in the brain of mice

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<i>S</i>-Mercuration of cellular proteins by methylmercury and its toxicological implications

Cited by 47 publications

References 126 publications

Fisetin impedes developmental methylmercury neurotoxicity via downregulating apoptotic signalling pathway and upregulating Rho GTPase signalling pathway in hippocampus of F1 generation rats

Fisetin impedes developmental methylmercury neurotoxicity via downregulating apoptotic signalling pathway and upregulating Rho GTPase signalling pathway in hippocampus of F1 generation rats

Selenocystine against methyl mercury cytotoxicity in HepG2 cells

Methylmercury induces the expression of TNF-α selectively in the brain of mice

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Resources

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Fisetin impedes developmental methylmercury neurotoxicity via downregulating apoptotic signalling pathway and upregulating Rho GTPase signalling pathway in hippocampus of F₁ generation rats

Fisetin impedes developmental methylmercury neurotoxicity via downregulating apoptotic signalling pathway and upregulating Rho GTPase signalling pathway in hippocampus of F₁ generation rats