Department of Pharmacology and Therapeutics, University of Dundee.
Br J Clin Pharmacol. 1974 Jun;1(3):191-5. doi: 10.1111/j.1365-2125.1974.tb00235.x.
1 The relationship between mechanical fragility, glutathione peroxidase inhibition and Heinz body formation, in erythrocytes exposed to oxidant drugs in vitro, has been investigated. All drugs tested caused Heinz body formation, and with the exception of acetyl salicylic acid and salicylic acid, also caused increased erythrocyte mechanical fragility. 2 There was a direct relationship between mechanical fragility and drug concentration. Mechanical fragility increased in parallel with Heinz body formation, with primaquine, gentisic acid, ascorbic acid and potassium chlorate. In contrast Heinz body formation occurred at drug concentrations which did not cause a marked increase in mechanical fragility in the case of menadione, acetyl phenylhydrazine and phenylhydrazine. 3 The degree of inhibition of glutathione peroxidase was directly related to increased mechanical fragility with menadione, gentisic acid and potassium chlorate. However other substances causing increased mechanical fragility resulted in little or no loss of glutathione peroxidase activity. 4 The results show that there is no constant relationship between mechanical fragility caused by drugs, the formation of Heinz bodies and the inhibition of glutathione peroxidase. The factors contributing to oxidant drug-induced haemolysis appear to be variable and depend upon the drug concerned.
已经研究了体外暴露于氧化剂药物的红细胞中机械脆性、谷胱甘肽过氧化物酶抑制和海因茨体形成之间的关系。所有测试的药物都导致海因茨体形成，除了乙酰水杨酸和水杨酸外，还导致红细胞机械脆性增加。
机械脆性与药物浓度之间存在直接关系。与 primaquine、gentisic acid、抗坏血酸和氯酸钾一样，机械脆性与海因茨体形成平行增加。相比之下，在 menadione、acetyl phenylhydrazine 和 phenylhydrazine 的情况下，海因茨体形成发生在不会导致机械脆性明显增加的药物浓度下。
谷胱甘肽过氧化物酶的抑制程度与 menadione、gentisic acid 和氯酸钾引起的机械脆性增加直接相关。然而，其他导致机械脆性增加的物质几乎没有或没有丧失谷胱甘肽过氧化物酶活性。
结果表明，药物引起的机械脆性、海因茨体形成和谷胱甘肽过氧化物酶抑制之间没有恒定的关系。氧化剂药物诱导的溶血的因素似乎是可变的，取决于相关的药物。
