Player T J, Mills D J, Horton A A
Br J Cancer. 1979 Jun;39(6):773-8. doi: 10.1038/bjc.1979.131.
NADPH- and ascorbic acid-induced microsomal lipid peroxidation was almost absent in subcutaneously implanted DAB-induced hepatomas D23, D30 and D192A, and present at greatly reduced levels in DAB-induced primary hepatomas when compared with normal liver controls. Fatty acid analysis of the microsomal lipid from passaged tumours demonstrated adequate levels of substrate in the phospholipid fractions to support lipid peroxidation. Lipid extracted from hepatoma microsomal fractions was shown to undergo ascorbic acid-induced lipid peroxidation, but to a lesser extent that the corresponding liver extract. This may be partially explained by a decrease in the phospholipid content of hepatoma microsomal membranes. However, phospholipid extracted from microsomal fractions of hepatoma and liver supported lipid peroxidation to a similar extent. The possible role of the non-lipid component of the membrane in the process of lipid peroxidation is discussed.
在皮下植入的二乙基亚硝胺(DAB)诱导的肝癌D23、D30和D192A中,NADPH和抗坏血酸诱导的微粒体脂质过氧化几乎不存在,与正常肝脏对照相比,DAB诱导的原发性肝癌中该过程的水平大幅降低。对传代肿瘤微粒体脂质的脂肪酸分析表明,磷脂组分中有足够水平的底物来支持脂质过氧化。从肝癌微粒体组分中提取的脂质显示会发生抗坏血酸诱导的脂质过氧化,但程度低于相应的肝脏提取物。这可能部分是由于肝癌微粒体膜磷脂含量的降低。然而,从肝癌和肝脏微粒体组分中提取的磷脂支持脂质过氧化的程度相似。文中讨论了膜的非脂质成分在脂质过氧化过程中的可能作用。