Juggi J S
Indian J Physiol Pharmacol. 1977 Oct-Dec;21(4):311-22.
Effects of CCL4 on bile formation and on the hepatic bilirubin metabolism were studied in rats by recording the intrabiliary pressure and flow rate, BSP and bilirubin clearances and by estimating the activity of the hepatic enzyme, Uridine diphosphate (UDP) glucuronyl transferase. From the results of these studies it was concluded that: (i) CCl4 reduced the rate of bile secretion by the lever cells of the rats, (ii) spontaneous bile flow and choleretic response to dehydrocholate declined in the CCl4 treated rats, (iii) CCl4 reduced the clearance of BSP and bilirubin (UCB or BG) at low plasma concentrations as well as the absolute rate of BSP and bilirubin (UCB or BG) excretion when plasma levels were above those required to saturate active transport of the dye or hepatic excretory mechanisms of bilirubin, (iv) CCl4 produced a specific bilirubin conjugatory defect by inhibiting the activity of hepatic UDP-glucuronyl transferase and that (v) all these hepatotoxic effects of CCl4 appeared as early as 2-3 hours after its administration.
通过记录胆管内压力和流速、BSP和胆红素清除率以及估算肝酶尿苷二磷酸（UDP）葡萄糖醛酸基转移酶的活性，研究了四氯化碳对大鼠胆汁形成和肝脏胆红素代谢的影响。从这些研究结果得出以下结论：（i）四氯化碳降低了大鼠肝实质细胞的胆汁分泌速率；（ii）在经四氯化碳处理的大鼠中，自发性胆汁流量和对脱氢胆酸盐的利胆反应下降；（iii）当血浆浓度低于染料主动转运或胆红素肝脏排泄机制饱和所需浓度时，四氯化碳降低了BSP和胆红素（未结合胆红素或结合胆红素）的清除率，以及当血浆水平高于该浓度时BSP和胆红素（未结合胆红素或结合胆红素）的绝对排泄速率；（iv）四氯化碳通过抑制肝脏UDP-葡萄糖醛酸基转移酶的活性产生了特异性胆红素结合缺陷；以及（v）四氯化碳的所有这些肝毒性作用在给药后2至3小时就最早出现。
