Cellular Conditions Responsible for Methylmercury-Mediated Neurotoxicity

Methylmercury (MeHg) is a widely known environmental pollutant that causes severe neurotoxicity. MeHg-induced neurotoxicity depends on various cellular conditions, including differences in the characteristics of tissues and cells, exposure age (fetal, childhood, or adulthood), and exposure levels. Research has highlighted the importance of oxidative stress in the pathogenesis of MeHg-induced toxicity and the site- and cell-specific nature of MeHg-induced neurotoxicity. The cerebellar granule cells and deeper layer cerebrocortical neurons are vulnerable to MeHg. In contrast, the hippocampal neurons are resistant to MeHg, even at high mercury accumulation levels. This review summarizes the mechanisms underlying MeHg-mediated intracellular events that lead to site-specific neurotoxicity. Specifically, we discuss the mechanisms associated with the redox ability, neural outgrowth and synapse formation, cellular signaling pathways, epigenetics, and the inflammatory conditions of microglia.

Automated summary

Methylmercury is an environmental pollutant that causes severe neurotoxicity. The neurotoxic effects of Methylmercury depend on various cellular conditions, including tissue and cell characteristics, exposure age, and exposure levels. This review summarizes the mechanisms underlying the site-specific neurotoxicity of Methylmercury, including oxidative stress, neural outgrowth, cellular signaling pathways, epigenetics, and microglial inflammation.