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.
Citation:
Zhang Yonggang,Chi Yanbang,Yang Tonghan.. EXPERIMENTAL STUDY ON THE CHANGE OF HEPATOCYTE MITOCHONDRIAL CALCIUM CONTENT AND LIVER LIPID-PEROXIDATION AFTER BILIARY OBSTRUCTION. CHINESE JOURNAL OF BASES AND CLINICS IN GENERAL SURGERY, 1999, 6(4): 210-212. doi:
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张永刚, 迟彦邦, 杨彤翰. 肝细胞钙超载与肝细胞损伤. 国外医学病理科学与临床分册, 1997; 17(3)∶255.
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Schmucker DL, Ohta M, Kanai S, et al. Hepatic injury induced by bile salts: correlation between biochemical and morphological events. Hepatology, 1990; 12(4)∶1216.
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Krahenbuhl S, Talos C, Fischer S, et al. Toxicity of bile acids on the electron transport chain of isolated rat liver mitochondria. Hepatology, 1994; 19(5)∶471.
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GonzalezFlecha B, Cutrin JC, Boveris A. Time and mechanism of oxidative stress and tissue damage in rat liver subjected to in vivo ischemiareperfusion. J Clin Invest, 1993; 91(1)∶564.
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Tsai LY, Lee KT, Tsai SM, et al. Changes of lipid peroxide levels in blood and liver tissue of patients with obsructive jaundice. Clinica Chimica Acta, 1993; 215(1)∶41.
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Sokol RJ, Mckim JMJ, Devereaux MK. Increased hydroperoxide generation during taurochenodeoxycholic acid (TCDC) toxicity in isolated rat hepatocytes. Gastroenterology, 1994; 106(1)∶A988.
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- 1. Aprille JR, Hom JA, Rulfs J, et al. Liver and skeletal muscle mitochondrial function following burn injury. J Trauma, 1977; 17(4)∶279.
- 2. Bradford MM. A rapid and sensitive method for the quantitation of microgram quantities of protein utilizing the principle of proteindye binding. Ann Biochem, 1976; 72∶248.
- 3. 岳平, 傅世英, 黄永麟等. 再灌注损伤心肌线粒体钙代谢与呼吸功能关系的研究. 中国病理生理杂志, 1991; (3)∶272.
- 4. Ohkawa H, Ohishi N, Yagi K. Assay for lipidperoxides in animal tissues by thiobarbituric acid reaction. Ann Biochem, 1979; 95(2)∶351.
- 5. 程迅生, 迟彦邦, 祁佐元. 慢性胆道梗阻时肝脏血流量及微血管床的变化. 中华外科杂志, 1992; 30(12)∶751.
- 6. 张永刚, 迟彦邦, 杨彤翰. 肝细胞钙超载与肝细胞损伤. 国外医学病理科学与临床分册, 1997; 17(3)∶255.
- 7. Schmucker DL, Ohta M, Kanai S, et al. Hepatic injury induced by bile salts: correlation between biochemical and morphological events. Hepatology, 1990; 12(4)∶1216.
- 8. Krahenbuhl S, Talos C, Fischer S, et al. Toxicity of bile acids on the electron transport chain of isolated rat liver mitochondria. Hepatology, 1994; 19(5)∶471.
- 9. GonzalezFlecha B, Cutrin JC, Boveris A. Time and mechanism of oxidative stress and tissue damage in rat liver subjected to in vivo ischemiareperfusion. J Clin Invest, 1993; 91(1)∶564.
- 10. Tsai LY, Lee KT, Tsai SM, et al. Changes of lipid peroxide levels in blood and liver tissue of patients with obsructive jaundice. Clinica Chimica Acta, 1993; 215(1)∶41.
- 11. Sokol RJ, Mckim JMJ, Devereaux MK. Increased hydroperoxide generation during taurochenodeoxycholic acid (TCDC) toxicity in isolated rat hepatocytes. Gastroenterology, 1994; 106(1)∶A988.