| Liver plays an important role in the metabolism and detoxification. This study investigated the influences of cerebral ischemia on liver antioxidation and the microsomal drug metabolism enzyme activity in rats. Focal cerebral ischemia in rats was produced by intraluminal suture to occlude the middle cerebral artery. The liver glutathione (GSH), glutathione S-transferase (GST), glutathione peroxidase (GSH-Px), glutathione reductase (GSH-Re), catalase (CAT), superoxide dismutase(SOD) and the content of malondialdehyde (MDA) and Ca2+ were assayed after cerebral ischemia 3h,12h and 24h. The liver GSH decreased slightly in ischemia 3h and decreased to 60% of the control(P<0.05) in ischemia 12h. GST increased to 156% of the control(P<0.0l) in ischemia 3h and after then retained a high level. Cerebral ischemia has no effect on liver GSH-Px and GSH-Re. The liver SOD and CAT significantly decreased after cerebral ischemia 3h, then retained a low level. The content of MDA and Ca2+ in liver mitochondrion increased to 172 %(P<0.01) and 270%(P<0.01), respectively, of the control after ischemia 12h. And in ischemia 12h the activity of alanine aminotransferase(ALT) and aspartate aminotransferase(AST) were also increased significantly. In conclusion, the change of the liver antioxidation may contribute to cerebral ischemia-induced liver injury.The total liver P450 content , erythromycin-N-demethylase and aniline hydroxylase were also evaluated. Total CYP content increased to 123% of control (P<0.05) and aniline hydroxylase activity increased to 167% of control (P<0.01)at 3h following cerebral ischemia. 12h after cerebral ischemia, total liver P450 content,erythromycin-N-demethylase and aniline hydroxylase activity have no distinct change campared with the control. At 24h following cerebral ischemia, aniline hydroxylase activity increased to 150% of control (P<0.05), and erythromycin-N-demethylase activity decreased to 50% of contol (P<0.01). Taken together, our results show that in the earlier of cerebral ischemia, the metabolic capability of liver was weakened, and the risk of hepatic toxicosis heightened.Altered expression of hepatic CYP2E1 by xenobiotic or physiological stimuli is largely mediated through transcriptional or posttranscriptional mechanisms that may include altered CYP2E1 mRNA stability. To study the mechanism of the induction of CYP2E1 after cerebral ischemia, the glucose and insulin in serum was determined and the liver CYP2E1 was assayed at the mRNA level with reverse transcriptase polymerase chain reaction (RT-PCR). The insulin and glucose all increased in ischemia 3h, and the glucose level was highly correlated with the enzyme activity of CYP2E1. CYP2E1 mRNA had no significant change. Our results lead us to propose that the induction of CYP2E1 may associated with a posttranscriptional mechanisms and may result from reduced glucose utilization. |
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