DiSilvestro R A, Carlson G P
Human Nutrition and Food Management, Ohio State University, Columbus 43210.
Toxicol Lett. 1992 Apr;60(2):175-81. doi: 10.1016/0378-4274(92)90272-l.
Inflammation, induced by turpentine (0.1 ml i.m.), protected against carbon tetrachloride (CCl4)-induced hepatotoxicity based on serum activities of sorbitol dehydrogenase. Inflammation was confirmed by elevated serum ceruloplasmin activities, and was associated with high hepatic levels of metallothionein, a zinc protein proposed to protect against CCl4-induced injury. Inflammation suppressed cytochrome P-450 activities, but this was not associated with protection against CCl4-promoted liver microsomal injury as assessed by glucose-6-phosphatase activity loss. Thus, protection against plasma membrane injury did not result primarily from depressed microsomal activation of CCl4. Each effect of inflammation reported here resembled effects of zinc injections. This similarity strengthens the hypothesis that metallothionein protects against CCl4-induced hepatic plasma membrane injury.
松节油（0.1毫升，肌肉注射）诱导的炎症，基于山梨醇脱氢酶的血清活性，对四氯化碳（CCl4）诱导的肝毒性具有保护作用。血清铜蓝蛋白活性升高证实了炎症的存在，并且炎症与肝脏中金属硫蛋白水平升高有关，金属硫蛋白是一种锌蛋白，被认为可以预防CCl4诱导的损伤。炎症抑制了细胞色素P - 450的活性，但这与通过葡萄糖-6-磷酸酶活性丧失评估的预防CCl4促进的肝微粒体损伤无关。因此，对质膜损伤的保护并非主要源于CCl4微粒体活化的抑制。此处报道的炎症的每种作用都类似于锌注射的作用。这种相似性强化了金属硫蛋白可预防CCl4诱导的肝质膜损伤这一假说。
