Abstract
We previously showed that at low concentrations (0.01-10 mu mol l) mercury (Hg) compounds (especially methylmercuric chloride) may act synergistically with physiological agonists to activate platelets and may also cause changes in blood coagulation in experimental animals. Result obtained in this study indicate that the activation of pig blood platelets by methylmercuric chloride (MMC) is not dependent on membrane receptors for fibrinogen and ADP. Furthermore, we have calculated that pig platelets take up approximately 13-fold more Hg than plasma proteins during incubation of platelet-rich plasma with MMC. These findings may explain the recently reported link between vascular events and Hg poisoning.
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