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Acute renal toxicity of sodium chlorate: Redox imbalance, enhanced DNA damage, metabolic alterations and inhibition of brush border membrane enzymes in rats
- Ali, Shaikh Nisar, Arif, Hussain, Khan, Aijaz Ahmed, Mahmood, Riaz
- Environmental toxicology 2018 v.33 no.11 pp. 1182-1194
- DNA, DNA damage, DNA fragmentation, adults, antioxidant activity, byproducts, carbohydrate metabolism, chlorine dioxide, crosslinking, dose response, drinking water, enzymes, glutathione, histology, humans, hydrogen peroxide, kidneys, laboratory animals, lipids, males, microvilli, nephrotoxicity, oral administration, oxidation, pulp and paper industry, rats, sodium chlorate, thiols, water pollution
- Sodium chlorate (NaClO₃) is widely used in paper and pulp industries and as a non‐selective herbicide. Humans can be exposed to NaClO₃ through contaminated drinking water due to its improper and unchecked usage in industries and as herbicide. NaClO₃ is also present as a major stable by‐product in drinking water that has been disinfected with chlorine dioxide. In this study, we have investigated the effect of a single acute oral dose of NaClO₃ on rat kidney. Adult male Wistar rats were divided into one control and four NaClO₃ treated groups that were orally given different doses of NaClO₃ and euthanized 24 hr after the treatment. Oral administration of NaClO₃ resulted in increased hydrogen peroxide levels, lipid, and protein oxidation while thiol and glutathione content and activities of brush border membrane enzymes were decreased in kidney in a NaClO₃ dose‐dependent manner. Significant alterations in the activities of enzymes involved in carbohydrate metabolism and antioxidant defense were also observed. Administration of NaClO₃ induced DNA fragmentation and increased DNA–protein cross‐linking. Histological studies showed marked damage in kidney from NaClO₃ treated animals. These results strongly suggest that NaClO₃ induces nephrotoxicity via redox imbalance that results in DNA and membrane damage, metabolic alterations and brush border membrane enzyme dysfunction.