Vitamin C Regulates Redox Homeostasis and Mitigates Potassium Bromate-Induced Oxidative Injury to Rat Intestine

Potassium bromate (KBrO₃), a probable human carcinogen, is generated as a disinfection by-product during ozonation of water and is also used as a flour maturing agent. It has been shown to induce oxidative damage and subsequent tissue-toxicity in individuals who get exposed to it. Previously, we have reported that KBrO₃ induces oxidative stress and subsequent intestinal toxicity, as is evident from DNA damage and the histological studies. In the present study, the protective efficacy of dietary antioxidant vitamin C on KBrO₃-induced intestinal toxicity has been explored. Administration of KBrO₃ led to a decrease (almost 1.5 fold) in the brush border membrane enzymatic activities. The oxidative reductive homeostasis of the intestine was greatly affected, as reflected by the severe alterations in the antioxidant enzymatic system, besides altering the carbohydrate metabolism too. There was also an increase in DNA damage (+1.5 fold) and DNA-protein cross-linking (+2 fold). However, pretreatment with vitamin C resulted in significant attenuation/modulation in all these parameters. The biochemical studies were supported by the histological studies showing extensive intestinal damage in KBrO₃-treated animals and greatly reduced tissue injury in the vitamin C + KBrO₃ group. These results show that vitamin C mitigates bromate-induced intestinal toxic insult and oxidative damage by improving antioxidant defense, tissue integrity, and energy metabolism and thus can be used as a therapeutic/protective agent against bromate and its related compounds.