Teschke R, Bolsen K, Landmann H, Goerz G
Biochem Pharmacol. 1983 Jun 1;32(11):1745-51. doi: 10.1016/0006-2952(83)90120-x.
To study the effect of experimental hepatic porphyria on the activities of hepatic alcohol metabolizing enzymes, female rats received a chow diet containing 0.05% hexachlorobenzene (HCB). After long-term HCB treatment for 60 days hepatic porphyria developed as evidenced by increased hepatic delta-aminolevulinic acid synthase activity and enhanced urinary excretion of delta-aminolevulinic acid, porphobilinogen and total porphyrins. Concomitantly, the activities of the hepatic microsomal ethanol oxidizing system (MEOS) were strikingly augmented by 213% (P less than 0.05) and 177% (P less than 0.01) when expressed per g of liver wet weight or per 100 g of body weight, respectively, whereas hepatic alcohol dehydrogenase activities remained virtually unchanged. Moreover, hepatic catalase showed only a trend for a slightly lower enzymic activity under these experimental conditions. The present data therefore show that experimental hepatic porphyria is associated with alterations of hepatic MEOS activities, which in turn may be a factor for the manifestation of human hepatic porphyrias in the course of alcohol consumption.
为研究实验性肝卟啉症对肝脏酒精代谢酶活性的影响,雌性大鼠食用含0.05%六氯苯(HCB)的普通饲料。经HCB长期处理60天后,肝脏卟啉症形成,表现为肝脏δ-氨基-γ-酮戊酸合成酶活性增加以及尿中δ-氨基-γ-酮戊酸、胆色素原和总卟啉排泄增多。同时,以每克肝脏湿重或每100克体重表示时,肝脏微粒体乙醇氧化系统(MEOS)的活性分别显著增加了213%(P<0.05)和177%(P<0.01),而肝脏乙醇脱氢酶活性基本保持不变。此外,在这些实验条件下,肝脏过氧化氢酶仅呈现酶活性略有降低的趋势。因此,目前的数据表明,实验性肝卟啉症与肝脏MEOS活性的改变有关,这反过来可能是人类肝卟啉症在饮酒过程中表现出来的一个因素。