Protective effects of tocopherol against warm water-induced nephropathy in mice: A biochemical and histological evaluation

Heat stress combined with physical activity can impair kidney function by inducing oxidative damage. Swimming in warm water presents a unique model for studying heat-induced nephropathy. This study evaluated the protective effects of vitamin E (tocopherol) against warm-water-induced renal dysfunction and histological damage in mice. Forty-two male mice were divided into seven groups, including control and experimental groups, with the latter exposed to swimming at either 23°C or 35°C, with or without tocopherol supplementation (100 mg/kg/day). After 35 days, serum, urine and renal samples were analyzed for kidney function markers, oxidative stress indicators and histopathological changes. High-Performance Liquid Chromatography (HPLC) was used for the evaluation of tocopherol accumulation in the renal tissues. Swimming at 23°C caused no significant renal impairment. However, mice swimming at 35°C exhibited increased serum creatinine, reduced estimated glomerular filtration rate (eGFR), elevated malondialdehyde (MDA), decreased superoxide dismutase (SOD) activity, and pronounced tubular necrosis and inflammation indicating acute kidney injury. Tocopherol supplementation in mice swimming at 35°C had beneficial effects on renal function parameters, decreased oxidative stress, and preserved renal histological structure. HPLC confirmed increased tocopherol accumulation in the renal tissues of the supplemented groups. Swimming at 23°C was physiologically safe; however, exposure to 35°C induced measurable renal injury in mice. Tocopherol demonstrated renoprotective effects against heat-induced nephropathy by reducing oxidative stress and maintaining renal structural integrity and function. These findings suggest that tocopherol may serve as a potential therapeutic candidate for individuals exposed to environmental or occupational heat stress.