Protective effects of Selenium (Se) on Chromium (VI) induced nephrotoxicity in adult rats

Soudani, Nejla; Sefi, Mediha; Amara, Ibtissem Ben; Boudawara, Tahia; Zeghal, Najiba

doi:10.1016/j.ecoenv.2009.10.002

Cited by 75 publications

(44 citation statements)

References 55 publications

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“…The exposure of rats to K 2 Cr 2 O 7 elicited an increase in carbonyl formation and sulfhydryl oxidation, indicating that aldehydes, resulting from lipid peroxidation, provoked protein oxidative damage as reported previously by Gul et al [30]. The co-administration of Se through the diet of K 2 Cr 2 O 7 -treated rats restored the protein carbonyl and sulfhydryl contents to near-normal values; this could be explained by the antiradical/ antioxidant and metal-chelating efficacy of this trace element [11,57,70].…”

Section: Discussionsupporting

confidence: 60%

Oxidative damage induced by chromium (VI) in rat erythrocytes: protective effect of selenium

et al. 2011

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Excess chromium (Cr) exposure is associated with various pathological conditions including hematological dysfunction. The generation of oxidative stress is one of the plausible mechanisms behind Cr-induced cellular deteriorations. The efficacy of selenium (Se) to combat Cr-induced oxidative damage in the erythrocytes of adult rats was investigated in the current study. Female Wistar rats were randomly divided into four groups of six each: group I served as controls which received standard diet, group II received in drinking water K(2)Cr(2)O(7) alone (700 ppm), group III received both K(2)Cr(2)O(7) and Se (0.5 Na(2)SeO(3) mg/kg of diet), and group IV received Se (0.5 mg/kg of diet) for 3 weeks. Rats exposed to K(2)Cr(2)O(7) showed an increase of malondialdehyde and protein carbonyl levels and a decrease of sulfhydryl content, glutathione, non-protein thiol, and vitamin C levels. A decrease of enzyme activities like catalase, glutathione peroxidase, and superoxide dismutase activities was also noted. Co-administration of Se with K(2)Cr(2)O(7) restored the parameters cited above to near-normal values. Therefore, our investigation revealed that Se was a useful element preventing K(2)Cr(2)O(7)-induced erythrocyte damages.

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Section: Discussionsupporting

confidence: 60%

Oxidative damage induced by chromium (VI) in rat erythrocytes: protective effect of selenium

et al. 2011

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“…In contrast to the described antioxidant enzymes, SOD activity increased with cisplatin treatment. Likewise, Salomon et al [40] and Soudani et al [41] reported that SOD activity was induced in response to oxidative stress induced renal failure. However, SOD is a primary antioxidant enzyme that can be induced by oxidative stress [41].…”

Section: Discussionmentioning

confidence: 99%

Benfotiamine Enhances Antioxidant Defenses and Protects against Cisplatin‐Induced DNA Damage in Nephrotoxic Rats

Harisa

2013

J Biochem & Molecular Tox

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The objective of the present study was to assess superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx), paraoxonase (PON1), glutathione reductase (GR), and catalase (CAT) activities ratio and their relationship with DNA oxidative damage in rats treated with cisplatin (3 mg/kg bwt/day) in the presence and absence of benfotiamine (100 mg/kg/day) for 25 days. Cisplatin-induced renal damage was evidenced by renal dysfunction and elevated oxidative stress markers. SOD activity and levels of nitric oxide, protein carbonyl, malondialdehyde, and 8-hydroxy-2'-deoxyguanosine were significantly increased by cisplatin treatment. Moreover, the ratios of GPx/GR, SOD/GPx, SOD/CAT, and SOD/PON1 were significantly increased compared to control. In contrast, glutathione levels were significantly decreased by cisplatin treatment. Simultaneous treatment of rats with cisplatin and benfotiamine ameliorate these variables to values near to those of control rats. This study suggests that benfotiamine can prevent cisplatin-induced nephrotoxicity by inhibiting formation reactive species of oxygen and nitrogen.

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“…The elevated creatinine level shows that damage of the glomerular function and tubular damage. 35 Uric acid is the major metabolic product of purine nucleotides. 36 Impairment in kidney function could probably occur via kidney oxidative damage.…”

Section: Discussionmentioning

confidence: 99%

Ameliorative Role of Melissa officinalis against Hepatorenal Toxicities of Organophosphorus Malathion in Male Rats

El-Raheem¹

2015

MOJT

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It has been confirmed that organophosphorus compounds OP altered glucose homeostasis. Considerable experimental and clinical evidences have contributed the beneficial effects of antioxidant compounds in plant extract on hepatorenal toxicity. The aim of this study was to evaluate whether Melissa officinalis extract, was able to ameliorative hepatorenal injury induced by organophosphorus Malathion. Malathion at 27mg/kg bw was administered to rats alone or in combination with Melissa officinalis extract at 200mg/kg bw. Malathion decreases feed intake and body weight as well as liver and kidneys weight. Moreover, Malathion increases the levels of various serum marker enzymes AST, ALT and ALP. A significant increase in the level of serum urea, uric acid and creatinine in response to ML treatment. As well as ML induced increase in MDA in liver and kidneys while induced decreases in the activities of SOD, GPx and CAT. Co-administration of malathion with Melissa officinalis extract resulted in restoration of all tested parameter. These results may be due to the significant increase recorded in acetylcholine esterase (Ach E) activity invivo after co administration of malathion and Melissa officinalis extract. In histological study of liver and kidney, Malathion induced damage in liver and kidneys. However, MO administration to ML-treated animals resulted in overall improvement in liver and kidneys damage, emphasizing its antioxidant role. In light of the available data, it can deduce that ML-induced lipid peroxidation, oxidative stress, liver and kidneys damage rats, and conjoint supplementation of MO has resulted in pronounced ameliorating effect in all tested parameter and histological picture of liver and kidney. MOJ Toxicology Research ArticleOpen Access Ameliorative role of melissa officinalis against hepatorenal toxicities of organophosphorus malathion in male rats 104Copyright: ©2015 Sief et al. Citation:Sief MM, Khalil FA, Abou-Arab AA, et al. Ameliorative role of melissa officinalis against hepatorenal toxicities of organophosphorus malathion in male rats.

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Protective effects of Selenium (Se) on Chromium (VI) induced nephrotoxicity in adult rats

Cited by 75 publications

References 55 publications

Oxidative damage induced by chromium (VI) in rat erythrocytes: protective effect of selenium

Oxidative damage induced by chromium (VI) in rat erythrocytes: protective effect of selenium

Benfotiamine Enhances Antioxidant Defenses and Protects against Cisplatin‐Induced DNA Damage in Nephrotoxic Rats

Ameliorative Role of Melissa officinalis against Hepatorenal Toxicities of Organophosphorus Malathion in Male Rats

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