Ali Fahad, Jyoti Smita, Fatima Ambreen, Khanam Saba, Naz Falaq, Siddique Yasir Hasan
Section of Genetics, Department of Zoology, Faculty of Life Sciences, Aligarh Muslim University, Aligarh, Uttar Pradesh, India.
Sci Pharm. 2016 Apr-Jun;84(2):361-77. doi: 10.3797/scipharm.1506-06. Epub 2015 Jul 26.
The present investigation was aimed at studying the possible role of curcumin against N-nitrosodiethylamine (NDEA)-induced toxicity in albino rats. Administration of NDEA to rats at a concentration of 0.1 mg/ml in drinking water ad libitum for 21 days produced toxicity in them, which was evident from histopathological changes in the rat livers, and increased levels of blood serum enzyme markers, i.e. aspartate transaminase, alanine transaminase, alkaline phosphatase, and lactate dehydrogenase. In addition, the levels of oxidative stress markers like lipid peroxidation (LPO), protein carbonyl (PCC), and glutathione-S-transferase (GST) activity were elevated and the total glutathione (GSH) content was reduced in the livers. The administration of curcumin to rats at concentrations of 10, 20, and 40 mg/ml in drinking water along with 0.1 mg/ml of NDEA for 21 days effectively suppressed NDEA-induced toxicity and also resulted in a dose-dependent reduction in the levels of blood serum enzyme markers (AST, ALT, ALP, and LDH). Moreover, LPO, PCC, and GST activity were reduced and the GSH level was increased upon the administration of curcumin along with NDEA. The results obtained for the comet assay in rat hepatocytes and blood lymphocytes showed a significant dose-dependent decrease in the mean tail length. The micronucleus assay performed on rat hepatocytes also showed a dose-dependent reduction in the frequency of micronucleated cells along with curcumin administration. These results suggest that curcumin has a protective role against NDEA-induced toxicity in albino rats.
本研究旨在探讨姜黄素对N-亚硝基二乙胺(NDEA)诱导的白化大鼠毒性的可能作用。以0.1 mg/ml的浓度将NDEA随意添加到大鼠饮用水中,持续21天,大鼠出现了毒性反应,这从大鼠肝脏的组织病理学变化以及血清酶标志物(即天冬氨酸转氨酶、丙氨酸转氨酶、碱性磷酸酶和乳酸脱氢酶)水平的升高可以明显看出。此外,肝脏中氧化应激标志物如脂质过氧化(LPO)、蛋白质羰基(PCC)和谷胱甘肽-S-转移酶(GST)活性升高,总谷胱甘肽(GSH)含量降低。以10、20和40 mg/ml的浓度将姜黄素添加到大鼠饮用水中,并与0.1 mg/ml的NDEA一起给药21天,有效抑制了NDEA诱导的毒性,还导致血清酶标志物(AST、ALT、ALP和LDH)水平呈剂量依赖性降低。此外,与NDEA一起给予姜黄素后,LPO、PCC和GST活性降低,GSH水平升高。在大鼠肝细胞和血液淋巴细胞中进行彗星试验得到的结果显示,平均尾巴长度显著呈剂量依赖性降低。对大鼠肝细胞进行的微核试验也显示,随着姜黄素的给药,微核细胞频率呈剂量依赖性降低。这些结果表明,姜黄素对白化大鼠NDEA诱导的毒性具有保护作用。