Methylmercury and developmental neurotoxicity: A global concern

Abstract

Methylmercury (MeHg) is a globally relevant environmental neurotoxic pollutant. Recent evidence from the Faroe Islands and Seychelles cohort studies suggest that maternal exposure to MeHg via consumption of contaminated fish and seafood results in transplacental exposure of the fetus to MeHg, seriously affecting fetal neurodevelopment. In birth cohorts, with mercury exposure below the existing tolerable weekly intake (1.3 μg/kg b.w., European Food Safety Authority) MeHg exposure associations to adverse neurodevelopmental effects have been observed. However, there are inconsistencies between studies, attributing confounding factors as the primary source of data variability. We summarize current knowledge of MeHg-mediated effects during nervous system development. Major molecular targets are thiols and selenols and, in particular, selenoenzymes, resulting in exacerbated oxidative stress–related damage. Generation of reactive oxygen species (ROS) is an underlying trigger for apoptosis. Low levels of MeHg can induce apoptotic death in cerebellar neurons, and MeHg can induce endoplasmic reticulum stress, disrupt calcium homeostasis, and cause mitochondrial disruption. At a cellular level, the effects of MeHg exposure involve the dysfunction of a myriad of neurodevelopment and neurobehavioral functions.