Sulfhydryl groups mercury exposure

Mercury interacts with sulfhydryl groups in vivo, inhibiting enzymes and altering cell membranes. The pattern of clinical intoxication from mercury depends to a great extent on the chemical form of the metal and the route and severity of exposure. 

After inhalation, 70-80% of metallic vapor is retained and absorbed. Little is taken up in the gastrointestinal tract, and less than 10% is absorbed. In the body, it is oxidized to mercuric mercury, which binds to reduced sulfhydryl groups. The kidney is the main depository following exposure to both metallic and mercuric mercury. In addition to other organs, it passes into the brain and fetus. 

Not much is known about the toxic effects of ethylmercury and most toxicologists have assumed that the toxic changes would be similar to that caused by methylmercury. These alterations in turn are very complex and depend on duration of exposure, dose, and the age of the individual. Mercury salts have a strong affinity for sulfhydryl groups and this is likely to play a role in effecting their neurotoxicity. Some in vitro studies indicate that oxidative stress leading to lipid peroxidation and DNA damage may also underlie the mechanism of toxicity. 

Once absorbed, metallic and inorganic mercury enter an oxidation-reduction cycle. Metallic mercury is oxidized to the divalent inorganic cation in the red blood cells and lungs of humans and animals. Evidence from animal studies suggests that the liver is an additional site of oxidation. Absorbed divalent cation from exposure to mercuric compounds can, in turn, be reduced to the metallic or monovalent form and released as exhaled metallic mercury vapor. In the presence of protein sulfhydryl groups, mercurous mercury (Hg+) disproportionates to one divalent cation (Hg+2) and one molecule at the zero oxidation state (Hg°). The conversion of methylmercury or phenylmercury into divalent inorganic mercury can probably occur soon after absorption, also feeding into the oxidation-reduction pathway. 

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