Pari L, Prasath A
Department of Biochemistry and Biotechnology, Faculty of Science, Annamalai University, Annamalainagar 608002, Tamilnadu, India.
Chem Biol Interact. 2008 May 28;173(2):77-83. doi: 10.1016/j.cbi.2008.02.010. Epub 2008 Mar 6.
Nickel (Ni), a major environmental pollutant, is known for its wide toxic manifestations. In the present study caffeic acid (CA), one of the most commonly occurring phenolic acids in fruits, grains and dietary supplements, was evaluated for its protective effect against the Ni induced oxidative damage in liver. In this investigation, Ni (20 mg/kg body weight) was administered intraperitoneally for 20 days to induce toxicity. CA was administered orally (15, 30 and 60 mg/kg body weight) for 20 days with intraperitoneal administration of Ni. Ni induced liver damage was clearly shown by the increased activities of serum hepatic enzymes namely aspartate transaminase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP), gamma glutamyl transferase (GGT) and lactate dehydrogenase (LDH) along with increased elevation of lipid peroxidation indices (thiobarbituric reactive acid substances (TBARS) and lipid hydroperoxides). The toxic effect of Ni was also indicated by significantly decreased levels of enzymatic (superoxide dismutase (SOD), catalase (CAT) glutathione peroxidase (GPx) and glutathione S-transferase (GST)) and non-enzymatic antioxidants (glutathione (GSH), vitamin C and vitamin E). CA administered at a dose of 60 mg/kg body weight significantly reversed the activities of hepatic marker enzymes to their near normal levels when compared with other two doses. In addition, CA significantly reduced lipid peroxidation and restored the levels of antioxidant defense in the liver. All these changes were supported by histological observations. The results indicate that CA may be beneficial in ameliorating the Ni induced oxidative damage in the liver of rats.
镍（Ni）是一种主要的环境污染物，以其广泛的毒性表现而闻名。在本研究中，对水果、谷物和膳食补充剂中最常见的酚酸之一咖啡酸（CA）对镍诱导的肝脏氧化损伤的保护作用进行了评估。在这项研究中，腹腔注射镍（20毫克/千克体重）20天以诱导毒性。在腹腔注射镍的同时，口服给予CA（15、30和60毫克/千克体重）20天。血清肝酶即天冬氨酸转氨酶（AST）、丙氨酸转氨酶（ALT）、碱性磷酸酶（ALP）、γ-谷氨酰转移酶（GGT）和乳酸脱氢酶（LDH）活性增加，同时脂质过氧化指数（硫代巴比妥酸反应性酸性物质（TBARS）和脂质氢过氧化物）升高，清楚地表明镍诱导了肝脏损伤。镍的毒性作用还表现为酶促抗氧化剂（超氧化物歧化酶（SOD）、过氧化氢酶（CAT）、谷胱甘肽过氧化物酶（GPx）和谷胱甘肽S-转移酶（GST））和非酶促抗氧化剂（谷胱甘肽（GSH）、维生素C和维生素E）水平显著降低。与其他两个剂量相比，以60毫克/千克体重的剂量给予CA可使肝脏标志物酶的活性显著恢复到接近正常水平。此外，CA显著降低了脂质过氧化，并恢复了肝脏中的抗氧化防御水平。所有这些变化都得到了组织学观察的支持。结果表明，CA可能有助于减轻镍诱导的大鼠肝脏氧化损伤。
