Effects of diallyl tetrasulhde on cadmiuminduced oxidative damage in the liver of rats
Effects of diallyl tetrasulhde on cadmiuminduced oxidative damage in the liver of rats
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DOI：
10.1177/0960327107073810
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发表时间：
2007-06-01
影响因子：
2.8
通讯作者：
Pari, L.
中科院分区：
文献类型：
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作者：
Murugavel, P.;Pari, L.
研究了大蒜提取物二烯丙基四硫化物（diallyl tetrasulfide，简称大蒜素）对镉（Cd）致小鼠肝损伤的保护作用。在这项研究中，镉（3毫克/公斤体重）皮下注射3周，以诱导毒性。连续3周经口灌胃镉（10、20和40 mg/kg体重），皮下注射镉（Cd）。镉诱导的肝损伤证明从血清肝酶，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的活性增加，脂质过氧化指数（硫代巴比妥酸反应物质和氢过氧化物）和蛋白质羰基在肝脏中的显着升高。镉中毒大鼠的总巯基，还原型谷胱甘肽（GSH），维生素C和维生素E的水平下降，伴随着镉的积累增加，并显着降低活性的超氧化物歧化酶，过氧化氢酶（CAT），谷胱甘肽过氧化物酶，谷胱甘肽-S-转移酶（GST），谷胱甘肽还原酶，葡萄糖-6-磷酸脱氢酶在肝脏中。与其他剂量（10和20 mg/kg体重）的顺铂相比，40 mg/kg体重的顺铂给药可显著恢复肝脏标志物酶的活性。此外，镉（40 mg/kg体重）显著降低了镉的积累和脂质过氧化水平，恢复了肝脏的抗氧化防御水平。组织学研究还表明，镉处理大鼠的肝细胞形态与轻度门静脉炎症的显着改善，导致管理的reclamation。我们的研究结果表明，在保护镉诱导的氧化损伤在肝脏中可能起着至关重要的作用。
The protective efficacy of diallyl tetrasulfide (DTS) from garlic on liver injury induced by cadmium (Cd) was investigated. In this study, Cd (3 mg/kg body weight) was administered subcutaneously for 3 weeks to induce toxicity. DTS was administered orally (10, 20 and 40 mg/kg body weight) for 3 weeks with subcutaneous (sc) injection of Cd. Cd-induced liver damage was evidenced from increased activities of serum hepatic enzymes, namely aspartate transaminase, alanine transaminase, alkaline phosphatase and lactate dehydrogenase, with significant elevation of lipid peroxidation indices (thiobarbituric acid reactive substances and hydroperoxides) and protein carbonyl groups in the liver. Rats subjected to Cd toxicity also showed a decline in the levels of total thiols, reduced glutathione (GSH), vitamin C and vitamin E, accompanied by an increased accumulation of Cd, and significantly decreased activities of superoxide dismutase, catalase (CAT), glutathione peroxidase, glutathione-S-transferase (GST), glutathione reductase, and glucose-6-phosphate dehydrogenase in the liver. Administration of DTS at 40 mg/kg body weight significantly normalised the activities of hepatic marker enzymes, compared to other doses of DTS (10 and 20 mg/kg body weight). In addition, DTS (40 mg/kg body weight) significantly reduced the accumulation of Cd and the level of lipid peroxidation, and restored the level of antioxidant defense in the liver. Histological studies also showed that administration of DTS to Cd-treated rats resulted in a marked improvement of hepatocytes morphology with mild portal inflammation. Our results suggest that DTS might play a vital role in protecting Cd-induced oxidative damage in the liver.