Abstract
Methylmercury (MeHg) is a global pollutant that easily bioaccumulates in the marine food chain. This can be a detriment for human populations that rely on seafood as a principle source of nutrition since MeHg is a neurotoxin that disrupts brain development and function. The neurotoxicity of MeHg has been linked to its hydrophobicity and soft acid properties which instil it with the capacity to diffuse freely across the blood brain barrier and bind strongly to soft bases like sulfur on cysteine residues in proteins. Despite this, there seems to be a latency period between MeHg exposure and adverse neurological outcomes. This may be attributed to the gradual bioconversion of MeHg to inorganic mercury (IHg). Empirical data show that the reactive oxygen species (ROS) drive the bioconversion of MeHg to iHg. In particular, superoxide anion is the principle ROS responsible for catalyzing the demethylation of MeHg. This bioconversion mostly takes place inside the matrix of mitochondria which preferentially accumulates MeHg due to its high cysteine content. Studies using “omic” approaches have shown that MeHg disrupts mitochondrial function, in particular energy metabolism and antioxidant defense. With increasing awareness of environmental stewardship, incidence of acute MeHg poisoning from industrial pollution has become rare. However, the scale of chronic exposure to lower dose of MeHg as a result of global pollution or occupational hazard has grown. The talk will discuss the roles of toxicologists in the development of environmental management plan for MeHg in the local and global context.
