The potential risk for methylmercury (MeHg) exposure to humans continues to be substantial. It is a concern not only for those exposed in excess, but for all fish-consuming individuals. The long-term consequences of acute or chronic low-dose MeHg exposure remain uncertain. Extreme MeHg exposure incidents have offered a glimpse of the mechanism of toxicity, and incited further research. Minamata and other high-level MeHg contamination incidents demonstrated the severe consequences of exposure, particularly to the developing nervous system. Although epidemiological studies have been incongruent, it is paramount that researchers obtain a fundamental grasp on mechanisms of toxic insult, particularly as it relates to dissemination of MeHg to the brain. MeHg excretion requires demethylation. This process is protracted in the central nervous system (CNS), rendering the brain particularly vulnerable to toxicity. Moreover, the relative ease with which MeHg crosses the blood-brain barrier reinforces residence in the brain. Distribution to cortical astrocytes and subsequent dysfunction precede MeHg-induced neurotoxicity. The mechanism(s) by which MeHg elicits toxicity are complex. It is most likely that the combined effects on glutamate cycling and oxidative stress ultimately cause MeHg-induced neurotoxicity. This chapter addresses contemporary issues on the continued health risks associated with this metal.
|Original language||English (US)|
|Title of host publication||Essential and Toxic Trace Elements and Vitamins in Human Health|
|Number of pages||8|
|State||Published - Jan 1 2020|
- Oxidative stress
ASJC Scopus subject areas