An evaluation of the protective role of α-tocopherol on free radical induced hepatotoxicity and nephrotoxicity due to chromium in rats

Abstract

Aim:To avert the health problems induced by many environmental pollutants, available antioxidants have been evaluated. The present study was aimed to investigate whether α-tocopherol could protect the hexavalent chromium (Cr VI)-induced peroxidation in the liver and kidney and to explore the underlying mechanism of the same.Materials and Methods:A total of 24 Wistar adult female rats were equally divided into four groups. Group 1 served as control while Groups 2 and 3 were administered K2Cr2O7(10 mg/kg b.wt. s.c. single dose). In addition to (Cr VI), Group 3 also received α-tocopherol (125 mg/kg, daily) by oral gavage for 14 days. Group 4 was maintained as α-tocopherol control (dose as above). At the end of 14 days, blood samples were drawn for hematology. Subsequently, all the rats were sacrificed to collect liver and kidney samples for assay of tissue peroxidation markers, antioxidant markers and functional markers and histopathology.Results:Administration of chromium (Cr VI) in Group 2 significantly (P < 0.05) reduced the antioxidant markers such as superoxide dismutase and reduced glutathione along with significant (P < 0.05) increase in peroxidation markers such as malondialdehyde and protein carbonyls in the liver and kidney as compared with other groups. The functional markers in serum such as total protein was decreased significantly (P < 0.05), whereas other functional markers viz. alanine transaminase, blood urea nitrogen and creatinine were increased significantly (P < 0.05) in Group 2 as compared with the other groups. Significant (P < 0.05) decrease in hemoglobin, packed cell volume, total erythrocyte count, mean corpuscular volume, mean corpuscular hemoglobin and total leukocyte count were observed in Cr VI treated Group 2 rats. Prominent pathological changes were observed in the liver and kidney of Group 2. Co-treatment with α-tocopherol in Group 3 rats significantly (P < 0.05) reversed the Cr VI induced changes. The parameters in the study in Group 4 did not differ as compared with Group 1.Conclusions:α–tocopherol exhibited protective effect against Cr VI-induced damage to the liver and kidney by inhibition of lipid peroxidation owing its antioxidant activity.

Simvastatin attenuates chromium-induced nephrotoxicity in rats

“…The results of the present study demonstrated that Cr (VI) produced dose–dependent adverse effects on rat kidney. Nephrotoxicity of Cr (VI) was reported by several investigators (1-5). Our findings along with others suggested that kidney is susceptible for Cr (VI)-induced toxicity.…”

“…Sahu et al found that subcutaneous injection of chromium (VI) resulted in histopathological alterations in the rat kidney (4). Balakrishnan et al reported that administration of chromium in rats significantly reduced the antioxidant markers such as superoxide dismutase and reduced glutathione (GSH) along with significant increase in peroxidation markers such as malondialdehyde (MDA) in the rat kidney as compared with control animals (5). Khan et al exhibited Cr (VI) produced injury in rat kidney (6).…”

Radical Scavenging Activity of Neolamarckia Cadamba (Roxb) Bosser in Nephrolithiasis Related Oxidative Stress

“…The lipid peroxidation (LPO) produced by hydrogen peroxide, superoxide anion and hydroxyl radicals which result in altered structural integrity of cell membrane, cell organelle and loss of essential fatty acids by the formation of peroxide products 27 . The increased kidney oxalate concentration in EG treated groups of animals shown to inhibit the catalase activity 28 .…”

Impact of the Humic Origin Supplement on the Antioxidant System of Rats Affected by Chromium (VI)

“…За тривалого надходження Cr(VI) з повітрям і питною водою відбувається порушення функцій дихальної, травної, видільної, кістково-м'язової, нервової та імунної систем, збільшується ризик розвитку злоякісних пухлин та пригнічення процесів ембріонального розвитку [4]. Відомо, що під час поступового відновлення Cr(VI) до Cr(ІІI) індукується оксидативний стрес, шляхом стимулювання продукції АФО, а накопичення продуктів вільнорадикальних реакцій викликає пригнічення функціональної активності антиоксидантної системи, зумовлюючи зміщення рівноваги в системі прооксиданти-антиоксиданти [5,6].…”