Ferrali M, Fulceri R, Benedetti A, Comporti M
Res Commun Chem Pathol Pharmacol. 1980 Oct;30(1):99-112.
Carbonyl compounds released during the NADPH-Fe dependent peroxidation of liver microsomal lipids and identified as 4-hydroxyalkenals (almost entirely as 4-hydroxynonenal) while inhibiting microsomal enzymes (such as glucose 6-phosphatase and aminopyrine demethylase) which are affected by lipid peroxidation, have no effect on microsomal NADPH-cytochrome c reductase. The latter enzyme activity is unaffected (or even increased) when liver microsomes are allowed to peroxidize in the NADPH-Fe dependent system. NADPH-cytochrome c reductase, contrary to the other enzymes, is similarly unaffected after CCl4 poisoning, that is in a situation in which peroxidation of membrane lipids of liver endoplasmic reticulum has been unequivocally demonstrated. It appears therefore that the effects exherted by lipid peroxidation or by 4-hydroxyalkenals originating from lipid peroxidation parallel the effects of CCl4 intoxication in vivo.
在肝脏微粒体脂质的NADPH - 铁依赖性过氧化过程中释放出的羰基化合物,被鉴定为4 - 羟基烯醛(几乎全部为4 - 羟基壬烯醛),在抑制受脂质过氧化影响的微粒体酶(如葡萄糖6 - 磷酸酶和氨基比林脱甲基酶)时,对微粒体NADPH - 细胞色素c还原酶没有影响。当肝脏微粒体在NADPH - 铁依赖性系统中发生过氧化时,后一种酶的活性不受影响(甚至增加)。与其他酶相反,在四氯化碳中毒后,即在内质网的膜脂质过氧化已被明确证实的情况下,NADPH - 细胞色素c还原酶同样不受影响。因此,脂质过氧化或源自脂质过氧化的4 - 羟基烯醛所产生的影响与体内四氯化碳中毒的影响相似。