Through dog models of common bile duct obstruction (BDO), the contents of liver superoxide dismutase (SOD) and malondialdehyde(MDA) were measured 2,3,4 and 5 weeks after BDO. Results indicated that the hepatic MDA content was increased 2 weeks after BDO as compared with control group (Ｐ＜0.01), the hepatic SOD content was decreased 3 weeks after BDO (Ｐ＜0.05). When bile duct obstructing, these changed were more serious. The results suggest that liver has little ability to eliminate the superoxide free radicals after BDO, whereas the lipid peroxidation products increase. It may be one of the mechanisms of liver damage after BDO.
To investigate the mechanisms of hepatic injury after biliary obstruction. After a rat model of complete biliary obstruction(CBO) was induced, hepatocyte mitochondria was isolated and the calcium content of mitochondria, the contents of liver malondialdyhyde (MDA) and superoxide dismutase (SOD), the levels of serum T-Bil, ALT, ALP and GGT were measured in each group. Results: After CBO, mitochondrial calcium content, liver MDA and serum T-Bil, ALT, ALP, GGT became increased progressively, compared with control group (Ｐ＜0.05); the liver SOD was decreased markedly (Ｐ＜0.05). Mitochondrial calcium content was highly positively correlated with liver MDA content, serum ALT and ALP, r values were 0.967, 0.924 and 0.919 respectively (Ｐ＜0.01). The liver MDA content was highly positively correlated with serum ALT and ALP, r values were 0.949 and 0.843 respectively (Ｐ＜0.01). Conclusions: Mitochondrial calcium overload and liver lipid peroxidation may be the important mechanisms of hepatic injury induced by biliary obstruction.
