4.6 Article

Role of diallyl tetrasulfide in ameliorating the cadmium induced biochemical changes in rats

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ENVIRONMENTAL TOXICOLOGY AND PHARMACOLOGY
卷 20, 期 3, 页码 493-500

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ELSEVIER
DOI: 10.1016/j.etap.2005.05.009

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diallyl tetrasulfide; cadmium; lipid peroxidation; plasma antioxidants

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Cadmium (Cd) is an ubiquitous environmental and occupational toxic metal concerned with a variety of adverse effects. The present study was under-taken to evaluate the role of diallyl tetrasulfide (DTS), an organosulfur compound in alleviating the Cd induced biochemical changes in male Wistar rats. During the experiment, rats were injected with Cd (3 mg/(kg day)) subcutaneously alone or with oral administration of DTS at different doses (10, 20 and 40 mg/(kg day)) for 3 weeks. In Cd treated rats, the activities of aspartate transaminase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP), lactate dehydrogenase (LDH) and gamma glutamyl transferase (GGT) were significantly increased in serum with elevated levels of bilirubin, urea and creatinine. The hemoglobin level and creatinine clearance were also significantly decreased in Cd treated rats. In addition, the levels of plasma lipid peroxidation markers: thiobarbituric acid reactive substances and lipid hydroperoxides were significantly increased while the levels of plasma reduced glutathione (GSH), Vitamins C and E were significantly decreased in Cd administered rats. Administration of DTS along with Cd significantly decreased the serum, liver and kidney markers towards near normal level in a dose dependent manner. DTS at a dose of 40 mg/(kg day) was highly effective when compared to other doses (10 and 20 mg/(kg day)). DTS also significantly reduced the accumulation of Cd in blood and tissues as well as decreased the level of lipid peroxidation markers with elevation of antioxidants in plasma. All these changes were accompanied by histological observations in liver. The obtained results demonstrated the beneficial effect of DTS in reducing the harmful effects of Cd. (c) 2005 Elsevier B.V. All rights reserved.

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