Intestinal microbiota protects against methylmercury-induced neurotoxicity
- PMID: 37973679
- DOI: 10.1007/s10534-023-00554-1
Intestinal microbiota protects against methylmercury-induced neurotoxicity
Abstract
Methylmercury (MeHg) remains a global public health issue because of its frequent presence in human food sources obtained from the water. The excretion of MeHg in humans occurs slowly with a biological half-time of 32-47 days. Short-term MeHg exposure may cause long-lasting neurotoxicity. The excretion through feces is a major route in the demethylation of MeHg. Accumulating evidence suggests that the intestinal microbiota plays an important role in the demethylation of MeHg, thereby protecting the host from neurotoxic effects. Here, we discuss recent developments on the role of intestinal microbiota in MeHg metabolism, based on in vitro cell culture experiments, experimental animal studies and human investigations. Demethylation by intestinal bacteria is the rate-limiting step in MeHg metabolism and elimination. The identity of bacteria strains responsible for this biotransformation is currently unknown; however, the non-homogenous distribution of intestinal microbiota may lead to different demethylation rates in the intestinal tract. The maintenance of intestinal barrier function by intestinal microbiota may afford protection against MeHg-induced neurotoxicity, which warrant future investigations. We also discuss studies investigating the effects of MeHg exposure on the population structural stability of intestinal microbiota in several host species. Although this is an emerging area in metal toxicity, current research suggests that a change in certain phyla in the intestinal microbiota may indicate MeHg overexposure.
Keywords: Biotransformation; Metabolism; Methylmercury; Microbiota; Neurotoxicity.
© 2023. The Author(s), under exclusive licence to Springer Nature B.V.
Conflict of interest statement
The authors declare no conflict of interest.
References
-
- Akiyama M, Unoki T, Yoshida E, Ding Y, Yamakawa H, Shinkai Y, Ishii I, Kumagai Y (2020) Repression of mercury accumulation and adverse effects of methylmercury exposure is mediated by cystathionine γ-lyase to produce reactive sulfur species in mouse brain. Toxicol Lett 330:128–133. https://doi.org/10.1016/j.toxlet.2020.05.007 - DOI - PubMed
-
- Amin-Zaki L, Elhassani S, Majeed MA, Clarkson TW, Doherty RA, Greenwood MR, Giovanoli-Jakubczak T (1976) Perinatal methylmercury poisoning in Iraq. Am J Dis Child 130(10):1070–1076. https://doi.org/10.1001/archpedi.1976.02120110032004 - DOI - PubMed
-
- Amin-zaki L, Majeed MA, Clarkson TW, Greenwood MR (1978) Methylmercury poisoning in Iraqi children: clinical observations over two years. Br Med J 1(6113):613–616. https://doi.org/10.1136/bmj.1.6113.613 - DOI - PubMed - PMC
-
- Amoroso C, Perillo F, Strati F, Fantini MC, Caprioli F, Facciotti F (2020) The role of gut microbiota biomodulators on mucosal immunity and intestinal inflammation. Cells. https://doi.org/10.3390/cells9051234 - DOI - PubMed - PMC
-
- Antunes Dos Santos A, Appel Hort M, Culbreth M, López-Granero C, Farina M, Rocha JB, Aschner M (2016) Methylmercury and brain development: a review of recent literature. J Trace Elem Med Biol 38:99–107. https://doi.org/10.1016/j.jtemb.2016.03.001 - DOI - PubMed
Publication types
MeSH terms
Grants and funding
LinkOut - more resources
Full Text Sources