Kanazawa K, Ashida H
Department of Agricultural Chemistry, Kobe University, Japan.
Int J Tissue React. 1991;13(5):225-31.
The relationship between the oxidative stress and inactivation of hepatic enzymes was examined in rats. An intake of lipid peroxidation products or pro-oxidative drugs provokes oxidative stress in the living body. Secondary peroxidation products of linoleic acid were administered orally, and the oxidative stress was evaluated by thiobarbituric acid (TBA) and haemoglobin-methylene blue (HMB) tests, and by the reduction in tocopherol level. A specific decrease in hepatic phosphoglucomutase activity was found following the oxidative stress caused by the dose with secondary products. Then, ten pro-oxidative drugs were administered intraperitoneally and the effects on the enzymatic activity were determined. Among the ten drugs, CCl4, alcohol, paraquat, phenobarbital, thiopental and methylcholanthrene caused the TBA values to increase, and the phosphoglucomutase activity to decrease, in the liver 24 h after the doses. It was attempted to clarify the inactivation mechanism by using parenchymal hepatocytes. When the cells were cultured in medium containing aldehydic products originating from lipid peroxidation, these aldehydes significantly suppressed the induction of phosphoglucomutase by dexamethasone as compared with the cells in aldehyde-free medium. We consider that aldehydes inhibit the hormonal induction of phosphoglucomutase in the rat liver.
在大鼠中研究了氧化应激与肝酶失活之间的关系。摄入脂质过氧化产物或促氧化药物会在生物体内引发氧化应激。口服亚油酸的二级过氧化产物，并通过硫代巴比妥酸（TBA）和血红蛋白-亚甲蓝（HMB）试验以及生育酚水平的降低来评估氧化应激。在用二级产物给药引起的氧化应激后，发现肝磷酸葡萄糖变位酶活性有特异性降低。然后，腹腔注射十种促氧化药物，并测定其对酶活性的影响。在这十种药物中，四氯化碳、酒精、百草枯、苯巴比妥、硫喷妥钠和甲基胆蒽给药24小时后，肝脏中的TBA值升高，磷酸葡萄糖变位酶活性降低。试图通过使用实质肝细胞来阐明失活机制。当细胞在含有源自脂质过氧化的醛类产物的培养基中培养时，与无醛培养基中的细胞相比，这些醛类显著抑制了地塞米松对磷酸葡萄糖变位酶的诱导。我们认为醛类抑制大鼠肝脏中磷酸葡萄糖变位酶的激素诱导。
