Mercury Toxicity - Mechanism

Mechanism

Mercury is highly reactive with selenium, an essential dietary element required by about 25 genetically distinct enzyme types (selenoenzymes). Among their numerous functions, selenoenzymes prevent and reverse oxidative damage in the brain and endocrine organs. The molecular mechanism of mercury toxicity involves its unique ability to irreversibly inhibit activities of selenoenzymes, such as thioredoxin reductase (IC50 = 9 nM). Although it has many additional functions, thioredoxin reductase restores vitamins C and E, as well as a number of other important antioxidant molecules, back into their reduced forms, enabling them to counteract oxidative damage within body cells. Since the rate of oxygen consumption is particularly high in brain tissues, production of reactive oxygen species (ROS) is accentuated in these vital cells, making them particularly vulnerable to oxidative damage and especially dependent upon the antioxidant protection provided by selenoenzymes. High mercury exposures deplete the amount of cellular selenium available for the biosynthesis of thioredoxin reductase and other selenoenzymes that prevent and reverse oxidative damage, which, if the depletion is severe and long lasting, results in brain cell dysfunctions that can ultimately cause death.

High exposures to mercury in its various forms are particularly toxic to fetuses and infants. Women who have been exposed to mercury in substantial excess of dietary selenium intakes during pregnancy are at risk of giving birth to children with serious birth defects. Mercury exposures in excess of dietary selenium intakes in young children can have severe neurological consequences, preventing nerve sheaths from forming properly. Mercury inhibits the formation of myelin.

According to some evidence, mercury poisoning may predispose to Young's syndrome (men with bronchiectasis and low sperm count).

Because of differences in tissue distributions, mercury poisoning's effects will differ depending on whether it has been caused by exposure to elemental mercury, inorganic mercury compounds (as salts), or organomercury compounds.