Tretter L, Nguyen T H, Szahados G, Horvath I
2nd Institute of Biochemistry, Semmelweis University, Medical School, Budapest, Hungary.
Biochem Biophys Res Commun. 1989 Aug 30;163(1):356-62. doi: 10.1016/0006-291x(89)92143-8.
Lipid peroxidation intensity is compared in Ehrlich Ascites Cell and in liver mitochondria, prepared from tumor bearing mice. Malondialdehyde formation is negligible in intact ascites tumour mitochondria, but it is significantly increased in permeabilised mitochondria and in isolated mitochondrial membranes. We suggest that the resistance against oxidative stress is a consequence of efficient protective mechanisms operating in the intact tumour mitochondria and the low level of polyunsaturated fatty acids under these circumstances cannot be the rate limiting factor in lipid peroxidation. Succinate, an effective inhibitor of mitochondrial lipid peroxidation in liver, cannot determine malondialdehyde formation in ascites tumour mitochondria.
比较了艾氏腹水癌细胞和荷瘤小鼠肝脏线粒体中的脂质过氧化强度。完整腹水肿瘤线粒体中丙二醛的形成可忽略不计,但在通透化线粒体和分离的线粒体膜中显著增加。我们认为,对氧化应激的抗性是完整肿瘤线粒体中有效保护机制起作用的结果,在这种情况下多不饱和脂肪酸含量低不可能是脂质过氧化的限速因素。琥珀酸是肝脏线粒体脂质过氧化的有效抑制剂,但不能决定腹水肿瘤线粒体中丙二醛的形成。