Ogiso T, Kobayashi T, Kuhara K, Kato Y
Jpn J Pharmacol. 1975 Aug;25(4):411-21.
The effect of "drugs for liver disease", protoporphyrin (PP) and phosphorylcholine (PC), on CCl4-induced liver injury was studied. Attention was given to the levels of microsomal drug-metabolizing enzyme and lipolytic enzyme activities and of some microsomal components such as phospholipid and peroxides. Administration of PP to CCl4-poisoned rats was found to increase the decreased microsomal drug-metabolizing enzyme activities, aminopyrine N-demethylase, aniline p-hydroxylase, cytochrome P-450 and b5 and lipolytic enzyme activity in CCl4-poisoned liver (12-20% increase as compared with those of the poisoned rats), and returned to control levels earlier than in CCl4-poisoned rats. Furthermore, administration of PP to CCl4-poisoned rats caused a decrease in the lipid peroxidation. A single dose of PP to normal rats was shown to increase these parameters, to a small extent. One of the mechanisms may be attributed to the fact that PP increases the biosynthesis of the hemoproteins by means of the incorporation of PP into the pigments and protects the membranes from lipid peroxides and the free radicals. On the other hand, administration of PC to the poisoned rats did not enhance the levels of the drug-metabolizing enzyme activities except for aminopyrine N-demethylase. Phospholipid phosphorous content, however, increased by 13-14% when PC was given. Thus, it is considered that PC may enhance the reconstitution of phospholipids in the injured membrane.
研究了“肝病药物”原卟啉(PP)和磷酸胆碱(PC)对四氯化碳诱导的肝损伤的影响。关注了微粒体药物代谢酶和脂解酶活性水平以及一些微粒体成分如磷脂和过氧化物的水平。发现给四氯化碳中毒的大鼠施用PP可增加四氯化碳中毒肝脏中降低的微粒体药物代谢酶活性、氨基比林N-脱甲基酶、苯胺对羟基化酶、细胞色素P-450和b5以及脂解酶活性(与中毒大鼠相比增加12 - 20%),并且比四氯化碳中毒大鼠更早恢复到对照水平。此外,给四氯化碳中毒的大鼠施用PP可导致脂质过氧化作用降低。给正常大鼠单次施用PP显示可在一定程度上增加这些参数。其中一个机制可能归因于PP通过将PP掺入色素中增加血红素蛋白的生物合成,并保护膜免受脂质过氧化物和自由基的损伤。另一方面,给中毒大鼠施用PC除了氨基比林N-脱甲基酶外,并未提高药物代谢酶活性水平。然而,当给予PC时,磷脂磷含量增加了13 - 14%。因此,认为PC可能增强受损膜中磷脂的重构。