Batra J K, Raj H G, Subramanian T A
Toxicon. 1987;25(3):345-9. doi: 10.1016/0041-0101(87)90263-7.
Cord factor (a mycobacterial toxin) treatment of mice for 72 hr resulted in decreased activities of hepatic drug metabolizing enzymes. The toxin treated animals exhibited reduced levels of liver cytochrome P-450 and cytochrome b5, accompanied by significant lowering of NADPH-cytochrome c reductase and NADH-cytochrome b5 reductase activities. The hepatic activities of aminopyrine N-demethylase and aniline hydroxylase were diminished, while liver cytosolic glutathione S-transferase activity was inhibited in mice receiving the toxin. Earlier studies from this laboratory (J. K. Batra, Ph.D. Thesis, Delhi University, India, 1982) on the effects of experimental tuberculosis on hepatic drug metabolism revealed changes similar to the presently reported influence of cord factor on mouse liver microsomal monooxygenases. Thus, the action of cord factor (on hepatic drug metabolism) largely mimics the effects of tuberculosis infection.
用索状因子(一种分枝杆菌毒素)处理小鼠72小时后,肝脏药物代谢酶的活性降低。经毒素处理的动物肝脏细胞色素P-450和细胞色素b5水平降低,同时NADPH-细胞色素c还原酶和NADH-细胞色素b5还原酶的活性显著降低。接受毒素的小鼠中,氨基比林N-脱甲基酶和苯胺羟化酶的肝脏活性降低,而肝脏胞质谷胱甘肽S-转移酶活性受到抑制。该实验室早期(J.K.巴特拉,博士论文,印度德里大学,1982年)关于实验性结核病对肝脏药物代谢影响的研究显示,其变化与目前报道的索状因子对小鼠肝脏微粒体单加氧酶的影响相似。因此,索状因子(对肝脏药物代谢)的作用在很大程度上模拟了结核感染的影响。