Abstract

The effects of methyl mercury on human blood platelets was studied. It induced platelet shape change, platelet aggregation, the platelet release reaction, and the synthesis of malondialdehyde. All of these effects were inhibited by indomethacin, a cyclooxygenase inhibitor. The release reaction and malondialdehyde generation could be induced in the absence of aggregation, and prostaglandin E₁ inhibited release but not malondialdehyde production. It is concluded that the activation of arachidonate cycloperoxidation is a plausible and adequate explanation for these effects of methyl mercury, and speculated that the toxic effects of methyl mercury are due to an analogous disturbance of lipid metabolism in other tissue. Methyl mercury also inhibited the prostaglandin E₁-stimulated adenylate cyclase of platelets; influenced the rate of uptake of adenosine, adenine, and serotonin, and had minor effects on adenine nucleotide metabolism.