Miura T, Muraoka S, Ogiso T
Department of Biochemistry, Hokkaido University of Pharmaceutical Sciences, Otaru, Japan.
Res Commun Mol Pathol Pharmacol. 1995 Feb;87(2):133-43.
Adriamycin (AD)-Fe3+ caused the inactivation of Na(+)-, K(+)-ATPase and Ca(2+)-ATPase of erythrocyte membranes during lipid peroxidation. AD-Fe3+ also induced the formation of fluorescent substances from the membranes with lipid peroxidation. The fluorescent substances were little extracted by chloroform-methanol, indicating that they were retained in the membranes. Butylated hydroxytoluene and trolox strongly inhibited both the inactivation of these ATPases and the formation of fluorescent substances with lipid peroxidation. Another antioxidant, vitamin E, slightly prevented the damage of the membranes. However, p-nitrophenyl phosphatase activity and acetylcholine esterase have lower or no susceptibility to the membrane lipid peroxidation. These results indicated that the ATPases were very sensitive to lipid peroxidation and that the membranes were modified during the peroxidation reaction.
阿霉素(AD)-Fe3+在脂质过氧化过程中导致红细胞膜的Na(+)-、K(+)-ATP酶和Ca(2+)-ATP酶失活。AD-Fe3+还诱导膜在脂质过氧化过程中形成荧光物质。这些荧光物质很少被氯仿-甲醇提取,表明它们保留在膜中。丁基羟基甲苯和生育三烯酚强烈抑制这些ATP酶的失活以及脂质过氧化过程中荧光物质的形成。另一种抗氧化剂维生素E略微防止了膜的损伤。然而,对硝基苯磷酸酶活性和乙酰胆碱酯酶对膜脂质过氧化的敏感性较低或不敏感。这些结果表明,ATP酶对脂质过氧化非常敏感,并且在过氧化反应过程中膜发生了改变。