Importance of mercury as toxic metal came into limelight after the incidence of Minamata disease in Japan (1953-1960).
At Minamata Bay in Japan many people lost their lives, many were permanently crippled and babies born to mothers consuming the mercury contaminated fish were genetically defective.
The source of mercury was the effluent discharged into the bay from a vinyl chloride plant, Minamata Chemical Company. The fish in the bay were found to contain 25 to 100 ppm mercury in the form of methyl mercury.
The Minamata incidence was followed by a tragic incidence in Iraq, where many people died consuming wheat contaminated with organic mercury used as fungicides for seed dressings (methyl mercury nitrite, methyl mercury chloride, etc.).
It is to be noted that all the forms of Hg are not toxic. Elemental Hg is relatively inert and non-toxic. However, due to its high vapour pressure, when inhaled it causes severe damage to the central nervous system.
Inorganic Hg is highly insoluble and also non-toxic. Mercurous ion (Hg2 2+) is low toxic but not mercuric ion (Hg2).
The toxicity of Hg2+ is due to its high affinity for sulphur atoms, by attaching itself to sulphur containing amino acids of protein, it forms bonds with hemoglobin and serum albumin containing sulphydryl groups.
The most toxic species are, however, organic mercury, especially CH3Hg+ as it is soluble in fat, lipid of membranes and brain tissue. The covalent Hg-C bond cannot be disrupted easily and thus, remains for a long time in the cells.
This, in turn, prohibits active transport of sugars, but allows passage of K to the membrane, resulting in energy deficiency in cells and disorder of central nervous system.