Neurotoxic mechanisms of methylmercury

Abstract

The general population is exposed to methylmercury (MeHg) through a diet, especially fishes. The ability of MeHg to easily pass through the biological membranes seems to be responsible for easily passing of MeHg through the blood brain barrier and the placental barrier. Thus, the accumulation of MeHg in the brain and in the fetus results in neurological disturbances and fetal impairments. The neuronal damage caused by MeHg is almost exclusively limited to the central nervous system in the adult human. Furthermore, the areas of damage to the brain are highly localized. Little is known about the mechanism of the selective damage caused by MeHg in the nervous system. In this paper, many studies on the adverse effects of MeHg at the biochemical level were cited. The ability to accumulate MeHg and a low level of intracellular glutathione seem to make neuronal cells to susceptible to MeHg. By considering the high affinity of MeHg cations to SH groups, it appears reasonable that a large number of cellular functions are being affected. Effects of MeHg on protein synthesis, membrane functions and cytoskeletons are discussed. Recent evidence suggests that oxidative stress and/or apoptosis are involved in the neurotoxicity of MeHg. Cumulative data indicate that functions of microtubules and neuronal transmission are highly susceptible toward MeHg exposure in vivo and in vitro. In prenatal exposure, a possible mechanism of MeHg toxicity is that MeHg alters the brain architecture and decreases the brain size due to the depression of cell division and neuronal migration, perhaps through inhibition of the microtubule functions.