Acute oral dose of sodium nitrite causes redox imbalance and DNA damage in rat kidney

• Published in: Journal of cellular biochemistry 2018-04, Vol.119 (4), p.3744-3754
• Main Authors: Ansari, Fariheen Aisha, Ali, Shaikh Nisar, Khan, Aijaz Ahmed, Mahmood, Riaz
• Format: Article
• Language: English
• Subjects: Animals; antioxidant capacity; Antioxidants; Bioassays; Body weight; Chemical modification; Comet assay; Damage; Damage detection; Deoxyribonucleic acid; DNA; DNA damage; Food additives; Glutathione; Hydrogen peroxide; Intermediates; Kidneys; Lipid peroxidation; Meat; Meat products; nitrite; Nitrites; Nucleotides; Oxidation; Oxidative stress; Peroxidation; Proteins; rat kidney; Rats; Rodents; Sodium; Sodium nitrite; Toxicity
• ISSN: 0730-2312; 1097-4644
• DOI: 10.1002/jcb.26611

Sodium nitrite (NaNO2) 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 NaNO2 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 NaNO2 at 20, 40, 60, and 75 mg/kg body weight; untreated rats served as the control group. All animals in NaNO2‐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 NaNO2 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 NaNO2‐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. Sodium nitrite (NaNO2) 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 NaNO2 on oxidative stress parameters, antioxidant capacity, and DNA in rat kidney. Our results suggest that nitrite induces nephrotoxicity in rats which is mediated through redox imbalance and results in DNA damage. Highlights Oral administration of sodium nitrite caused oxidative damage to rat kidney. Non‐enzymatic oxidative stress parameters were altered and antioxidant capacity was decreased. Activities of membrane‐bound enzymes were altered. An increase in DNA damage was observed.