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Acute oral dose of sodium nitrite causes redox imbalance and DNA damage in rat kidney
Author(s) -
Ansari Fariheen Aisha,
Ali Shaikh Nisar,
Khan Aijaz Ahmed,
Mahmood Riaz
Publication year - 2018
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.26611
Subject(s) - sodium nitrite , oxidative stress , nitrite , chemistry , glutathione , comet assay , lipid peroxidation , nephrotoxicity , antioxidant , kidney , dna damage , preservative , dna oxidation , biochemistry , 8 hydroxy 2' deoxyguanosine , lipid peroxide , pharmacology , dna , toxicity , endocrinology , food science , biology , enzyme , organic chemistry , nitrate
Sodium nitrite (NaNO 2 ) is widely used as a food additive and preservative in fish and meat products. We have evaluated the effect of a single acute oral dose of NaNO 2 on oxidative stress parameters, antioxidant capacity, and DNA in rat kidney. Male Wistar rats were divided into four groups and given single oral dose of NaNO 2 at 20, 40, 60, and 75 mg/kg body weight; untreated rats served as the control group. All animals in NaNO 2 ‐treated groups showed marked alterations in various parameters of oxidative stress as compared to the control group. This included increase in lipid peroxidation, protein oxidation, hydrogen peroxide levels, and decrease in reduced glutathione content and antioxidant capacity. Administration of NaNO 2 also increased DNA damage as evident from release of free nucleotides and confirmed by comet assay. It also led to greater cross‐linking of DNA to proteins. Histological analysis showed marked morphological changes in the kidney of NaNO 2 ‐treated animals. These alterations could be due to increased free radical generation or direct chemical modification by reaction intermediates. Our results suggest that nitrite‐induced nephrotoxicity is mediated through redox imbalance and results in DNA damage.