No abstract

Potassium bromate (KBrO3) is widely used as a food additive and is a major water disinfection by-product. It induces multiple organ toxicity in humans and experimental animals and is a probable human carcinogen. The present study reports the protective effect of dietary antioxidant taurine on KBrO3-induced damage to the rat intestine. Animals were randomly divided into four groups: control, KBrO3 alone, taurine alone and taurine+ KBrO3. Administration of KBrO3 alone led to decrease in the activities of intestinal brush border membrane enzymes while those of antioxidant defence and carbohydrate metabolism were also severely altered. There was increase in DNA damage and DNA-protein cross-linking. Treatment with taurine, prior to administration of KBrO3, resulted in significant attenuation in all these parameters but the administration of taurine alone had no effect. Histological studies supported these biochemical results showing extensive intestinal damage in KBrO3-treated animals and greatly reduced tissue injury in the taurine+ KBrO3 group. These results show that taurine ameliorates bromate induced tissue toxicity and oxidative damage by improving the antioxidant defence, tissue integrity and energy metabolism. Taurine can, therefore, be potentially used as a therapeutic/protective agent against toxicity of KBrO3 and related compounds.

Industrialization and unchecked use of nitrate/nitrite salts for various purposes has increased human exposure to high levels of sodium nitrite (NaNO2) which can act as a pro-oxidant and pro-carcinogen. Oral exposure makes the gastrointestinal tract particularly susceptible to nitrite toxicity. In this work, the effect of administration of a single acute oral dose of NaNO2 on rat intestine was studied. Animals were randomly divided into four groups and given single doses of 20, 40, 60 and 75 mg NaNO2/kg body weight. Untreated animals served as the control group. An NaNO2 dose-dependent decline in the activities of brush border membrane enzymes, increase in lipid peroxidation, protein oxidation, hydrogen peroxide levels and decreased thiol content was observed in all treated groups. The activities of various metabolic and antioxidant defense enzymes were also altered. NaNO2 induced a dose-dependent increase in DNA damage and DNA-protein crosslinking. Histopathological studies showed marked morphological damage in intestinal cells. The intestinal damage might be due to nitrite-induced oxidative stress, direct action of nitrite anion or chemical modification by reaction intermediates.

Sodium chlorate (NaClO) is a widely used non-selective herbicide. It is also generated as a byproduct during disinfection of drinking water by chlorine dioxide. In the present work, the effects of NaClO on human erythrocytes were studied under in vitro conditions. Incubation of erythrocytes with different concentrations of NaClO at 37 °C for 90 min resulted in significant hemolysis. Cell lysates were prepared from NaClO-treated and untreated (control) erythrocytes and assayed for various biochemical parameters. Methemoglobin levels were significantly increased and methemoglobin reductase activity was reduced upon NaClO treatment. There was a significant increase in protein oxidation and lipid peroxidation with a decrease in reduced glutathione and total sulfhydryl content. This suggests the induction of oxidative stress in erythrocytes upon exposure to NaClO. The occurrence of oxidative stress was confirmed by significantly increased generation of reactive oxygen species and lowered antioxidant response of the cells. NaClO treatment also increased nitric oxide levels showing induction of nitrosative stress. The activities of major antioxidant and membrane-bound and metabolic enzymes were significantly altered upon incubation of erythrocytes with NaClO. The erythrocytes became more osmotically fragile while electron microscopic images showed gross morphological alterations in NaClO-treated cells. These results show that NaClO induces oxidative stress in human erythrocytes, which results in extensive membrane damage and lowers the antioxidant response.

Sodium nitrite (NaNO ) 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 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 at 20, 40, 60, and 75 mg/kg body weight; untreated rats served as the control group. All animals in NaNO -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 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 -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.