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蓝藻藻红蛋白对四氯化碳诱导的大鼠毒性的改善作用。

Ameliorative action of cyanobacterial phycoerythrin on CCl(4)-induced toxicity in rats.

作者信息

Soni Badrish, Visavadiya Nishant P, Madamwar Datta

机构信息

BRD School of Biosciences, Sardar Patel Maidan, Vadtal Road, Satellite Campus, Post Box 39, Sardar Patel University, Vallabh Vidyanagar 388120, Gujarat, India.

出版信息

Toxicology. 2008 Jun 3;248(1):59-65. doi: 10.1016/j.tox.2008.03.008. Epub 2008 Mar 18.

DOI:10.1016/j.tox.2008.03.008
PMID:18440118
Abstract

Carbon tetrachloride (CCl(4)) is largely used as solvent in chemical industries. Carbon tetrachloride is also well known for hepatic and renal toxic actions. The in vivo metabolism of carbon tetrachloride to trichloromethyl (CCl(3)) and peroxy trichloromethyl (OOCCl(3)) radicals has been extensively reported to cause acute liver damage like cirrhosis, steatosis and necrosis. We have evaluated protective action of purified cyanobacterial phycoerythrin (C-PE) on carbon tetrachloride-induced hepatic and renal toxicity in male rats. Rats were orally treated with 25 and 50mg/kg BW of C-PE along with CCl(4) (50% CCl(4), 0.5 ml/kg BW, intraperitoneally) for 28 consecutive days. Results demonstrated that C-PE dose-responsively ameliorates CCl(4)-toxicity by significantly decreasing (P<0.05) organs weight, aminotransferases, alkaline phosphatase, glucose, lipid profile, creatinine, uric acid and malondialdehyde (MDA) concentrations with rise in body weight, food intake, hemoglobin, protein, bilirubin and FRAP values. Neither C-PE nor CCl(4) influenced on serum minerals. Hepatic and renal tissues showed significant decline (P<0.05) in malondialdehyde, lipid hydroperoxides and conjugated dienes with rise in SOD, catalase, GPx, GSH, vitamin-E and vitamin-C levels. Presently observed pharmacological effect on CCl(4) toxicity were from tetrapyrrole molecule and to some extent bilirubin biotransformations, as well as metabolic (dietary protein) actions of C-PE.

摘要

四氯化碳(CCl₄)在化学工业中大量用作溶剂。四氯化碳还因其对肝脏和肾脏的毒性作用而广为人知。四氯化碳在体内代谢为三氯甲基(CCl₃)和过氧三氯甲基(OOCCl₃)自由基,这已被广泛报道会导致急性肝损伤,如肝硬化、脂肪变性和坏死。我们评估了纯化的蓝藻藻红蛋白(C-PE)对四氯化碳诱导的雄性大鼠肝毒性和肾毒性的保护作用。大鼠连续28天口服25和50mg/kg体重的C-PE,同时腹腔注射CCl₄(50% CCl₄,0.5 ml/kg体重)。结果表明,C-PE呈剂量依赖性地改善CCl₄毒性,通过显著降低(P<0.05)器官重量、转氨酶、碱性磷酸酶、葡萄糖、血脂、肌酐、尿酸和丙二醛(MDA)浓度,同时体重、食物摄入量、血红蛋白、蛋白质、胆红素和FRAP值升高。C-PE和CCl₄均未影响血清矿物质。肝组织和肾组织中丙二醛、脂质氢过氧化物和共轭二烯显著下降(P<0.05),同时超氧化物歧化酶、过氧化氢酶、谷胱甘肽过氧化物酶、谷胱甘肽、维生素E和维生素C水平升高。目前观察到的对CCl₄毒性的药理作用来自四吡咯分子,在一定程度上来自胆红素生物转化以及C-PE的代谢(膳食蛋白质)作用。

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