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首页> 外文期刊>Journal of applied toxicology >Oral administration of diphenyl diselenide potentiates hepatotoxicity induced by carbon tetrachloride in rats.
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Oral administration of diphenyl diselenide potentiates hepatotoxicity induced by carbon tetrachloride in rats.

机译：口服二苯二硒化物可增强四氯化碳对大鼠的肝毒性。

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Carbon tetrachloride (CCl(4)) is a model for studying free radical-induced liver injury and screening hepato-protective drugs. Numerous studies have reported the involvement of oxidative stress in CCl(4)-induced liver damage and the hepato-protective effects mediated by different antioxidants. The present study examined the effects of diphenyl diselenide, (PhSe)(2), on hepatotoxicity induced by CCl(4 )in rats. To this end, male Wistar rats received (PhSe)(2) by oral route at the dosage of 31.2 mg/kg for one or two days. After the second day of treatment, rats received CCl(4) orally in a single dose. The liver and kidney were utilized for determination of histopathology, biochemical [aspartate (ALT) and alanine (AST) aminotransferases, alkaline phosphatase (ALP), total bilirrubin (TB) and gamaglutamyl transferase (GGT)] and toxicological parameters [thiobarbituric reactive species (TBARS) levels, catalase activity, ascorbic acid, nonprotein thiols (NPSH) and aminolevulinate dehydratase (delta-ALA-D) activity]. Repeated administration of (PhSe)(2 )caused a marked potentiation of hepatotoxicity induced by CCl(4 )exposure, as manifested by an increase in biochemical parameters (AST, ALT, ALP, GGT and BT) and severe alteration in histopathology. This study also demonstrated a potentiation of TBARS levels and a consequent depletion of important antioxidant defenses including catalase and ascorbic acid. Pre-treatment with a single dose of (PhSe)(2 )prevented the effect of strychnine, a substrate for CYPs, abolishing lethality in mice. This result indicates that (PhSe)(2) prevented animal death, suggesting an activator action of (PhSe)(2) in CYPs. This study clearly indicates that (PhSe)(2 )potentiated acute hepatic damage induced by CCl(4). Copyright (c) 2008 John Wiley & Sons, Ltd.
机译：四氯化碳（CCl（4））是研究自由基诱导的肝损伤和筛选肝保护药物的模型。大量研究报告了氧化应激参与CCl（4）诱导的肝损伤和由不同抗氧化剂介导的肝保护作用。本研究检查了二苯基二硒化物（PhSe）（2）对CCl（4）诱导的大鼠肝毒性的影响。为此，雄性Wistar大鼠经口服途径以31.2 mg / kg的剂量接受（PhSe）（2）一两天。在治疗的第二天后，大鼠口服单剂量的CCl（4）。肝脏和肾脏用于确定组织病理学，生化[天冬氨酸（ALT）和丙氨酸（AST）氨基转移酶，碱性磷酸酶（ALP），总胆红素（TB）和伽马谷氨酰转移酶（GGT）]和毒理学参数[硫代巴比妥反应性物种（TBARS）水平，过氧化氢酶活性，抗坏血酸，非蛋白硫醇（NPSH）和氨基乙酰丙酸酯脱水酶（δ-ALA-D）活性]。重复给药（PhSe）（2）导致CCl（4）暴露诱导的肝毒性显着增强，这表现为生化参数（AST，ALT，ALP，GGT和BT）的增加以及组织病理学的严重改变。这项研究还证明了TBARS的增强作用以及随之而来的重要抗氧化剂防御系统（包括过氧化氢酶和抗坏血酸）的消耗。用单剂量的（PhSe）（2）进行预处理可预防士的宁（一种用于CYP的底物）的作用，从而消除了小鼠的致死性。该结果表明（PhSe）（2）防止了动物死亡，表明（PhSe）（2）在CYP中具有激活作用。这项研究清楚地表明（PhSe）（2）增强了CCl（4）诱导的急性肝损伤。版权所有（c）2008 John Wiley＆Sons，Ltd.

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