Maintenance of mitochondrial function by astaxanthin protects against bisphenol A-induced kidney toxicity in rats

Abstract

Bisphenol A (BPA), a global environmental pollutant, has been reported to have the potential to induced organs toxicity. This study explored the potential benefits of astaxanthin (ATX), a natural antioxidant, against BPA toxicity in the kidney, and explored whether mitochondria are involved in this condition. Male Wistar rats were fed with a vehicle, BPA, BPA plus ATX, ATX and were evaluated after five weeks. ATX treatment significantly reversed BPA-induced changes in body weight, kidney/body weight, and renal function related markers. When treated simultaneously with ATX, the imbalance of the oxidative-antioxidant status caused by BPA was also alleviated. The high expression of BPA-induced pro-inflammatory cytokines were inhibited by ATX treatment. ATX treatment also lessened the effects of BPA-induced caspase-3, -8, -9 and -10 gene expression and enzyme activity. The benefits of ATX were associated with enhanced mitochondrial function, which led to increased mitochondrial-encoded gene expression, mitochondrial copy number, and increased mitochondrial respiratory chain complex enzyme activity. Our results demonstrate the efficacy of ATX in protecting BPA-induced kidney damage, in part by regulating oxidative imbalance and improving mitochondrial function. Collectively, these findings provide a new perspective for the rational use of ATX in the treatment of BPA-induced kidney disease.