Ally A I, Miller D R
Prostaglandins Leukot Med. 1984 Aug;15(2):209-21. doi: 10.1016/0262-1746(84)90178-1.
It has been reported that the addition of nonaggregating concentrations of collagen, epinephrine, thrombin or arachidonic acid to platelets potentiate their responses to subsequent subthreshold concentrations of aggregating agents. We have previously reported that low concentrations of methylmercury will potentiate human platelet ATP secretion and that this effect is blocked by aspirin. Using rat platelets we have examined the effect of low concentrations of methylmercury on the metabolism of arachidonic acid. Low concentrations of methylmercury (20-100 microM) inhibit washed platelet lipoxygenase activity. In experiments using platelet rich plasma a higher concentration of methylmercury was required to produce a comparable inhibition of arachidonic acid metabolism. At these concentrations no inhibition of platelet thromboxane synthetase was seen. These findings suggest that methylmercury potentiates platelet aggregation and secretion by reducing the inhibitory effect of 12 HPETE on thromboxane biosynthesis.
据报道，向血小板中添加非聚集浓度的胶原蛋白、肾上腺素、凝血酶或花生四烯酸会增强它们对随后低于阈值浓度的聚集剂的反应。我们之前报道过，低浓度的甲基汞会增强人血小板ATP的分泌，并且这种效应会被阿司匹林阻断。我们使用大鼠血小板研究了低浓度甲基汞对花生四烯酸代谢的影响。低浓度的甲基汞（20 - 100微摩尔）会抑制洗涤过的血小板脂氧合酶活性。在使用富含血小板血浆的实验中，需要更高浓度的甲基汞才能对花生四烯酸代谢产生类似的抑制作用。在这些浓度下，未观察到对血小板血栓素合成酶的抑制作用。这些发现表明，甲基汞通过降低12 - HPETE对血栓素生物合成的抑制作用来增强血小板聚集和分泌。
