Literature DB >> 22827614

Protective effects of α-tocopherol against oxidative stress related to nephrotoxicity by monosodium glutamate in rats.

M V Sauganth Paul1, M Abhilash, Mathews V Varghese, Manju Alex, R Harikumaran Nair.   

Abstract

CONTEXT: Chronic oral intake of high doses of monosodium glutamate (MSG) could be harmful to tissues and organs. Oxidative stress enhances membrane damage by lipid peroxidation and alterations of antioxidant enzymes, which affects the functional activity of organs. Antioxidant vitamins have the capacity to regulate the oxidative stress related functional and pathological processes.
OBJECTIVE: In this study, the protective role of α-tocopherol against MSG-induced nephrotoxicity was analyzed.
MATERIALS AND METHODS: MSG (4 g/kg) was given orally to female wistar rats for a period of 180 days. Renal function parameters (urea, uric acid, and creatinine), lipid peroxidation markers (malondialdehyde and conjugated dienes), antioxidant system (superoxide dismutase, catalase, glutathione peroxidase, glutathione transferase, and reduced glutathione), and histopathology were investigated. All tests were done in rats treated with MSG and at two different doses of α-tocopherol (100 and 200 mg/kg).
RESULTS: Oral exposure of MSG significantly increased renal function markers, lipid peroxidation byproducts, and altered antioxidant system. Moreover, the kidney showed congested glomeruli, tubular swelling, capillary congestion and microhemorrhages in stromal areas of the tubules. Co-administration of MSG and α-tocopherol (200 mg/kg) significantly reduced the oxidative damage compared with MSG-treated group and also restored the normal renal function. DISCUSSION: The results indicated that oxidative stress was involved in MSG-induced functional and pathological changes in the kidney. α-tocopherol modulates the functional disorder and maintains the normal architecture of renal tissue by reducing oxidative stress.
CONCLUSION: The α-tocopherol may be a potent protective agent in combating MSG-induced renal toxicity.

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Year:  2012        PMID: 22827614     DOI: 10.3109/15376516.2012.714008

Source DB:  PubMed          Journal:  Toxicol Mech Methods        ISSN: 1537-6516            Impact factor:   2.987


  17 in total

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