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Advances in Molecular Studies of Mercury Toxicity

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Toxicology".

Deadline for manuscript submissions: closed (30 April 2024) | Viewed by 817

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Department of Veterinary Integrative Biosciences (VIBS), School of Veterinary Medicine and Biomedical Sciences, Texas A&M University, College Station, TX 77843-4458, USA
Interests: toxicology; reproductive toxicology; developmental toxicology
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Special Issue Information

Dear Colleagues, 

Mercury, a highly toxic heavy metal, is a ubiquitous contaminant in our environment. There are three forms of mercury: elemental, inorganic and organic. Each mercury form presents unique aspects of toxicity and differs in its mechanism of transport and distribution in the body. It is known that interactions with sulfhydryl groups, oxidative stress induction and disruption of calcium ion homeostasis are critical mechanisms that confer toxicity to mercury. However, many aspects of mercury toxicity are still unknown. Fetuses and children are particularly susceptible to mercury toxicity due to its adverse effects on fetal growth, neurological development and cardiovascular function. Furthermore, there is considerable concern about the adverse consequences resulting from chronic exposure to low levels of mercury.

Previous reports have indicated that heavy metals, including mercury, regulate numerous genes, and mercury exposure influences a range of mechanisms in biological systems at the molecular and cellular levels. This Special Issue focuses on the scientific study of genetic and molecular determinants of susceptibility to mercury exposure and its toxic effects. An additional focus of this Special Issue is the assessment of new and novel countermeasures and treatments for mercury toxicity in adult and developing organisms.

Prof. Dr. Louise C. Abbott
Guest Editor

Manuscript Submission Information

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Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

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Keywords

  • mercury
  • methylmercury
  • toxicity
  • cells
  • tissues
  • signaling molecules
  • molecular determinants
  • genetic susceptibility
  • developmental susceptibility

Published Papers (1 paper)

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Research

12 pages, 2790 KiB  
Article
Methylmercury Induces Apoptosis in Mouse C17.2 Neural Stem Cells through the Induction of OSGIN1 Expression by NRF2
by Naoya Yamashita, Marino Uchiyama, Ryota Yamagata and Gi-Wook Hwang
Int. J. Mol. Sci. 2024, 25(7), 3886; https://doi.org/10.3390/ijms25073886 - 30 Mar 2024
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Abstract
Methylmercury is a known environmental pollutant that exhibits severe neurotoxic effects. However, the mechanism by which methylmercury causes neurotoxicity remains unclear. To date, we have found that oxidative stress-induced growth inhibitor 1 (OSGIN1), which is induced by oxidative stress and DNA damage, is [...] Read more.
Methylmercury is a known environmental pollutant that exhibits severe neurotoxic effects. However, the mechanism by which methylmercury causes neurotoxicity remains unclear. To date, we have found that oxidative stress-induced growth inhibitor 1 (OSGIN1), which is induced by oxidative stress and DNA damage, is also induced by methylmercury. Therefore, in this study, we investigated the relationship between methylmercury toxicity and the induction of OSGIN1 expression using C17.2 cells, which are mouse brain neural stem cells. Methylmercury increased both OSGIN1 mRNA and protein levels in a time- and concentration-dependent manner. Moreover, these increases were almost entirely canceled out by pretreatment with actinomycin D, a transcription inhibitor. Furthermore, similar results were obtained from cells in which expression of the transcription factor nuclear factor erythroid 2-related factor 2 (NRF2) was suppressed, indicating that methylmercury induces OSGIN1 expression via NRF2. Methylmercury causes neuronal cell death by inducing apoptosis. Therefore, we next investigated the role of OSGIN1 in methylmercury-induced neuronal cell death using the activation of caspase-3, which is involved in apoptosis induction, as an indicator. As a result, the increase in cleaved caspase-3 (activated form) induced by methylmercury exposure was decreased by suppressing OSGIN1, and the overexpression of OSGIN1 further promoted the increase in cleaved caspase-3 caused by methylmercury. These results suggest, for the first time, that OSGIN1 is a novel factor involved in methylmercury toxicity, and methylmercury induces apoptosis in C17.2 cells through the induction of OSGIN1 expression by NRF2. Full article
(This article belongs to the Special Issue Advances in Molecular Studies of Mercury Toxicity)
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