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Mercury, Environment and Health

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

Deadline for manuscript submissions: closed (31 October 2021) | Viewed by 3073

Special Issue Editor


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Guest Editor
UMR CNRS 5805 EPOC, University of Bordeaux, Arcachon Marine Station, Place du Dr Peyneau, 33120 Arcachon, France
Interests: environmental research

Special Issue Information

Dear Colleagues,

As you know, three main forms of mercury (Hg) concern toxicologists: elementary Hg and inorganic and organic Hg (methyl- (Me) and ethyl-Hg, thiomersal). Extensive knowledge about Hg toxicology has been developed in these last decades. Yet, several questions are still pending:

  • Is there a placental barrier against MeHg present at low environmentally relevant concentrations in food, as suggested by a recent study (Cambier et al., Food Chem Toxicol, 2018, 122:11-20)?
  • Is the fetal-to-mother blood Hg ratio a proof of higher accumulation of Hg in fetal organs?
  • Does this ratio rather reflect the greater affinity of fetal hemoglobin for MeHg compared to maternal hemoglobin and the fact that MeHg chelated by fetal hemoglobin does not allow MeHg accumulation in fetal organs (and is rather destined for excretion via the biliary tract)?
  • Therefore, what could be the blood circulating mercurial species—and the molecules or proteins they are chelated to— that accumulate in the organs (fetal or adult) of mammals, birds, reptiles, amphibians, and invertebrates?
  • What are the selenomercurial species formed in terrestrial mammals and other animals, besides those known in cetaceans?
  • Do mercurial species from polluted environments have a role in the spread of emergent diseases such as multiple sclerosis, autism, Alzheimer’s and Parkinson’s diseases, and autoimmune diseases?

Other important issues are still being debated, and there is a need to update our knowledge in their regard:

  • The huge gap between regulatory limits, for instance, the tolerable weekly intake and the reallowest-observed-adverse-effect level (LOAEL);
  • The role of selenoneine in the protection against the various forms of Hg;
  • The reason why bacteria devoid of the mer operon are 100 to 1000 times more sensitive to Hg(II) and MeHg than to other heavy metals such as Cd(II), Co(II), Ni(II), Pb(II), and Zn(II);
  • New findings and development on the topic of Hg contamination of vaccines and dental amalgams.

The issues raised above do not pretend to be comprehensive, and proposals from authors and colleagues will be welcome.

Colleagues and authors are invited to submit their manuscripts to this Special Issue.

Prof. Dr. Jean-Paul Bourdineaud
Guest Editor

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Keywords

  • methylmercury
  • divalent mercury
  • elementary mercury
  • fish
  • dental amalgams
  • vaccines
  • selenoneine
  • selenomercurial species
  • bacteria
  • bioavailable mercurial species

Published Papers (1 paper)

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Research

11 pages, 1507 KiB  
Article
DHA and Its Metabolites Have a Protective Role against Methylmercury-Induced Neurotoxicity in Mouse Primary Neuron and SH-SY5Y Cells
by Ami Oguro, Kenta Fujita, Yasuhiro Ishihara, Megumi Yamamoto and Takeshi Yamazaki
Int. J. Mol. Sci. 2021, 22(6), 3213; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22063213 - 22 Mar 2021
Cited by 12 | Viewed by 2531
Abstract
The consumption of fish now involves a risk of methylmercury (MeHg) exposure but also provides the benefit of ω-3 polyunsaturated fatty acids (ω-3 PUFAs) such as docosahexaenoic acid (DHA). Some epidemiological studies have suggested that the intake of DHA can alleviate the neurotoxicity [...] Read more.
The consumption of fish now involves a risk of methylmercury (MeHg) exposure but also provides the benefit of ω-3 polyunsaturated fatty acids (ω-3 PUFAs) such as docosahexaenoic acid (DHA). Some epidemiological studies have suggested that the intake of DHA can alleviate the neurotoxicity of MeHg, but the underlying mechanism is not known. Herein, we observed that pretreatment with 0.1–1 µM DHA suppressed MeHg-induced cytotoxicity in human neuroblastoma (SH-SY5Y) cells and mouse primary neuronal cells. These effects of DHA were canceled in the presence of the retinoid X receptor (RXR) antagonist UVI3003. An RXR agonist, bexarotene, suppressed the cytotoxicity of MeHg. DHA also suppressed the MeHg-induced production of reactive oxygen species (ROS) via an induction of antioxidant genes (catalase and SOD1). Pretreatment with DHA did not change the incorporation of MeHg. We showed previously that in the brain, the intake of DHA increased the level of 19,20-DHDP, which is the metabolite produced by cytochrome P450 and soluble epoxide hydrolase from DHA. In the present study, we observed that 19,20-DHDP also suppressed neurotoxicity from MeHg. These results indicate that DHA and its metabolites have a protective role in MeHg-induced neurotoxicity. Full article
(This article belongs to the Special Issue Mercury, Environment and Health)
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