Renugadevi J, Prabu S Milton
Department of Zoology, Faculty of Science, Annamalai University, Annamalainagar 608 002, Tamil Nadu, India.
Exp Toxicol Pathol. 2010 Mar;62(2):171-81. doi: 10.1016/j.etp.2009.03.010. Epub 2009 May 5.
This experiment pertains to the protective role of naringenin against cadmium (Cd)-induced oxidative stress in the liver of rats. Cadmium is a major environmental pollutant and is known for its wide toxic manifestations. Naringenin is a naturally occurring citrus flavonone which has been reported to have a wide range of pharmacological properties. In the present investigation cadmium (5mg/kg) was administered orally for 4 weeks to induce hepatotoxicity. Liver damage induced by cadmium was clearly shown by the increased activities of serum hepatic marker enzymes namely aspartate transaminase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP), lactate dehydrogenase (LDH), gamma glutamyl transferase (GGT) and serum total bilirubin (TB) along with the increased level of lipid peroxidation indices (thiobarbituric acid reactive substances (TBARS) and lipid hydroperoxides) and protein carbonyl contents in liver. The toxic effect of cadmium was also indicated by significantly decreased levels of enzymatic antioxidants (superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione S-transferase (GST)) and non-enzymatic antioxidants (reduced glutathione (GSH), vitamin C and vitamin E). Administration of naringenin at a dose of (50mg/kg) significantly reversed the activities of serum hepatic marker enzymes to their near-normal levels when compared to Cd-treated rats. In addition, naringenin significantly reduced lipid peroxidation and restored the levels of antioxidant defense in the liver. The histopathological studies in the liver of rats also showed that naringenin (50mg/kg) markedly reduced the toxicity of cadmium and preserved the normal histological architecture of the tissue. The present study suggested that naringenin may be beneficial in ameliorating the cadmium-induced oxidative damage in the liver of rats.
本实验探讨了柚皮素对镉（Cd）诱导的大鼠肝脏氧化应激的保护作用。镉是一种主要的环境污染物，以其广泛的毒性表现而闻名。柚皮素是一种天然存在的柑橘类黄酮，据报道具有广泛的药理特性。在本研究中，口服给予镉（5mg/kg）4周以诱导肝毒性。镉诱导的肝损伤表现为血清肝标志物酶即天冬氨酸转氨酶（AST）、丙氨酸转氨酶（ALT）、碱性磷酸酶（ALP）、乳酸脱氢酶（LDH）、γ-谷氨酰转移酶（GGT）和血清总胆红素（TB）的活性增加，同时肝脏中脂质过氧化指标（硫代巴比妥酸反应性物质（TBARS）和脂质氢过氧化物）和蛋白质羰基含量增加。镉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（还原型谷胱甘肽（GSH）、维生素C和维生素E）水平显著降低。与镉处理的大鼠相比，给予剂量为（50mg/kg）的柚皮素可使血清肝标志物酶的活性显著恢复至接近正常水平。此外，柚皮素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。大鼠肝脏的组织病理学研究还表明，柚皮素（50mg/kg）显著降低了镉的毒性，并保留了组织的正常组织结构。本研究表明，柚皮素可能有助于改善镉诱导的大鼠肝脏氧化损伤。
