Abstract
Introduction: The kidney is a major organ for nickel induced toxicity. Objectives: The purpose of this investigation was to determine the protective impact of vitamin E on nickel sulfate (NiSO4 ) caused kidney dysfunction in rats using biochemical and histopathological approaches. Materials and Methods: Adult male Wistar rats were selected as animal models and randomly divided into four groups (five rats in each group) as follows; group 1. The animals received orally (gavage) 250 mg/kg vitamin E (dissolved in corn oil) 30 minutes before inhalation exposure to1mg NiSO4 /m3 . This experiment was performed for 6 hours daily for 10 consecutive days. Group 2; the rats received by gavage corn oil (vehicle) 30 minutes before inhalation exposure to1mg NiSO4 /m3 . This experiment was performed for 6 hours daily for 10 consecutive days. Group 3; animals of this group were given by gavage 250 mg/kg vitamin E only (without exposure to NiSO4 ) for 10 consecutive days. Group fourth were received by gavage an equal volume of vehicle (corn oil) for 10 consecutive days. All animals were killed 24 hours after the last treatments with sodium pentobarbital. Kidney tissues were removed. One part of the tissues were used for glutathione (GSH) and malondialdehyde (MDA) determination, other parts were fixed and processed for light microscopy. Results: The levels of MDA significantly increased and GSH decreased in rats exposed to NiSO4 in comparison to those in non-exposed rats. Histopathological observations also indicated that NiSO4 induced damage in the kidney. Additionally, administration of vitamin E prior to exposure to NiSO4 markedly decreased renal damage-induced by NiSO4 . Conclusion: The study showed that respiratory inhalation of NiSO4 induced oxidative stress and caused cell damage in rats’ kidney. Vitamin E effectively alleviated Ni-induced nephrotoxicity in rats. These observations suggest that vitamin E may have a protective effect against Ni-induced oxidative stress in the rats’ kidney.
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