2,4-Dichlorophenoxyacetic acid induced hepatic and renal toxicological perturbations in rat model: Attenuation by selenium supplementation.

Abstract

2,4-Dichlorophenoxyacetic acid (2,4-D) is a commercially used herbicide to manage broadleaf weeds that have various toxicological and ecological effects. In view of ever-escalating use of 2,4-D, risk assessment becomes mandatory to ensure the safety of both human health and the ecosystem. Oxidative injury has been expected as a possible mechanism implicated in 2,4-D toxicity. The present study was planned and conducted to explore the antioxidant potential of selenium (Se) supplementation to moderate the 2,4-D hepatic and renal toxicity in a rat model. The rats were randomly assigned to four equal groups and treated via oral gavage for a period of 4 weeks. Group I: received deionized water as a vehicle, group II: received 2,4-D (150 mg-1 kg-1 day-1), group III: received Se supplement (1 mg-1 kg-1 day-1), and group IV: received 2,4-D (150 mg-1 kg-1 day-1) and Se supplement (1 mg-1 kg-1 day-1) simultaneously. After 4 weeks of administration, 2,4-D induced toxicity was observed, as manifested by disrupted levels of plasma urea, creatinine, alkaline phosphatase (ALP), aspartate aminotransferase (AST), and alanine aminotransferase (ALT). Further, 2,4-D caused a considerable increase in tissue malondialdehyde (MDA) levels and decreased activity of antioxidant enzymes, including superoxide dismutase, catalase, and glutathione reductase. Se supplementation exhibited its antioxidant properties by significantly improving urea, creatinine, ALP, AST, and ALT, and MDA levels and antioxidant enzyme activities. In conclusion, the results suggest that 2,4-D induced hepatic and renal toxicities were attenuated by Se supplementation probably owing to its antioxidant properties.