Advances on the Influence of Methylmercury Exposure during Neurodevelopment

Mercury (Hg) is a toxic heavy-metal element, which can be enriched in fauna and flora and transformed into methylmercury (MeHg). MeHg is a widely distributed environmental pollutant that may be harmful to fish-eating populations through enrichment of aquatic food chains. The central nervous system is a primary target of MeHg. Embryos and infants are more sensitive to MeHg, and exposure to MeHg during gestational feeding can significantly impair the homeostasis of offspring, leading to long-term neurodevelopmental defects. At present, MeHg-induced neurodevelopmental toxicity has become a hotspot in the field of neurotoxicology, but its mechanisms are not fully understood. Some evidence point to oxidative damage, excitotoxicity, calcium ion imbalance, mitochondrial dysfunction, epigenetic changes, and other molecular mechanisms that play important roles in MeHg-induced neurodevelopmental toxicity. In this review, advances in the study of neurodevelopmental toxicity of MeHg exposure during pregnancy and the molecular mechanisms of related pathways are summarized, in order to provide more scientific basis for the study of neurodevelopmental toxicity of MeHg.

Automated summary

This review summarizes the advances in the study of neurodevelopmental toxicity caused by mercury exposure during pregnancy, as well as the molecular mechanisms of related pathways. Exposure to methylmercury during gestation can lead to long-term neurodevelopmental defects in embryos and infants, and the mechanisms behind it are not fully understood. Current evidence suggests that oxidative damage, excitotoxicity, calcium ion imbalance, mitochondrial dysfunction, epigenetic changes, and other molecular mechanisms play important roles in methylmercury-induced neurodevelopmental toxicity.