Watanabe A, Nakatsukasa H, Kobayashi M, Nagashima H
Acta Med Okayama. 1984 Oct;38(5):453-9. doi: 10.18926/AMO/30347.
Carbon tetrachloride (CCl4)-induced hepatotoxicity was potentiated by pretreatment with beta-phenethyl alcohol, abundantly present in sake. The injury was determined by serum GPT levels and histological examination. Similar results were observed in ethanol- and phenobarbital-pretreated rats. Acetaminophen-induced hepatotoxicity was not accentuated by beta-phenethyl alcohol or ethanol pretreatment. The activities of liver microsomal enzymes, such as cytochrome P-450, cytochrome b5 reductase, aniline hydroxylase and aminopyrine demethylase, were not altered in beta-phenethyl alcohol-pretreated rats. Thus, CCl4-induced hepatotoxicity potentiation by beta-phenethyl alcohol administration is postulated to be due to a mechanism other than increased free radical generation.
四氯化碳（CCl4）诱导的肝毒性可因用β-苯乙醇预处理而增强，β-苯乙醇在清酒中大量存在。通过血清谷丙转氨酶（GPT）水平和组织学检查来确定损伤情况。在乙醇和苯巴比妥预处理的大鼠中也观察到了类似结果。对乙酰氨基酚诱导的肝毒性不会因β-苯乙醇或乙醇预处理而加重。在β-苯乙醇预处理的大鼠中，肝脏微粒体酶如细胞色素P-450、细胞色素b5还原酶、苯胺羟化酶和氨基比林脱甲基酶的活性没有改变。因此，推测β-苯乙醇给药增强CCl4诱导的肝毒性是由于自由基生成增加以外的机制。
