Leoncini G, Poggi M
Istituto Policattedra di Chimica Biologica, Università di Genova, Italy.
Cell Biochem Funct. 1996 Jun;14(2):89-95. doi: 10.1002/cbf.655.
Methylglyoxal generates a slight increase in the basal level of hydrogen peroxide in platelets. The oxidation effect of methylglyoxal significantly potentiated by thrombin, depends on both the ketoaldehyde and the agonist concentrations. A further significant increase in hydrogen peroxide accumulation was obtained in platelets pretreated with the alkylating agent N-ethylmaleimide which depletes GSH and blocks glutathione peroxidase. Resting platelets completely transform the ketoaldehyde into D(-)lactate, whereas stimulated platelets transform about 10-15 per cent of the metabolized methylglyoxal into D(-)lactate. The metabolic modifications generated by methylglyoxal such as the GSH depletion and hydrogen peroxide accumulation induce modifications in platelet function. Methylglyoxal inhibits platelet aggregation induced by several agonists and ATP release induced by thrombin.
甲基乙二醛会使血小板中过氧化氢的基础水平略有升高。凝血酶能显著增强甲基乙二醛的氧化作用，这取决于酮醛和激动剂的浓度。在用耗尽谷胱甘肽（GSH）并阻断谷胱甘肽过氧化物酶的烷基化剂N - 乙基马来酰亚胺预处理的血小板中，过氧化氢的积累进一步显著增加。静息血小板可将酮醛完全转化为D（-）乳酸，而受刺激的血小板则将约10 - 15%代谢的甲基乙二醛转化为D（-）乳酸。甲基乙二醛产生的代谢改变，如谷胱甘肽耗尽和过氧化氢积累，会引起血小板功能的改变。甲基乙二醛可抑制多种激动剂诱导的血小板聚集以及凝血酶诱导的ATP释放。
