Abstract
Potassium bromate (PB) is a well-known additive in the food industry and a byproduct of water treatment. Its long-term exposure to any form of life exerts mild to severe toxic insults in a dose-dependent fashion and can even trigger carcinogenesis. This study examines the ameliorative effectiveness of a prominent polyphenol, naringenin (NIR), in rodents previously exposed to PB. The Swiss albino rats were assigned to five treatment groups (n = 5): Group I was the control, and Groups II and III were administered with PB alone (100 mg/kg) and NIR alone (2 mg/kg), respectively. The remaining two groups were treated with NIR at 2 and 4 mg/kg in the PB-preadministered rats. The animals were sacrificed after the treatment course to retrieve their liver and blood for biochemical, molecular, and histological studies. The PB-treated Group II showed a marked rise in liver function and toxicity markers in the serum samples, confirming hepatotoxicity after treatment. Disrupted redox markers (GSH and MDA) and compromised antioxidant enzymes (SOD and CAT) further support the hepatotoxicity induced by PB. Notably, NIR exhibited minimal toxicity, as indicated by Group III, and most of the measured parameters' values were comparable to those of the control. However, the combination groups (IV and V) showed improvement in the PB-mediated hepatotoxicity assessment dose-dependently. In addition, a prominent decline in LDH activity, concomitant with fan-like comet formation in the nuclear DNA, is observed in these groups, suggesting that NIR promotes apoptosis concurrently with reducing necrosis. The histopathological investigation further consolidates these findings, showing marked structural restoration in liver histology, along with improved activity of antioxidant enzymes and a more favorable redox status. Hence, NIR can be utilized in consumer products with PB as an ingredient or to reduce hepatotoxicity induced by PB or similar compounds or potential drugs in vivo.