Bisphenol A impairs mitochondrial function in spleens of mice via oxidative stress

Increasing evidences show that bisphenol A(BPA) affects immune responses, which the mechanism is mainly regarded as estrogenic effect on a variety of immune cells. Besides its estrogenic activity, BPA can cause oxidative damage of liver, kidneys and brain. Due to limited information concerning the effect of BPA on spleen, a principle site for initiation of primary immune responses, especially no data are available on its actions on the mitochondrial functions of spleen. To assess this effect, C57BL/6 female mice were exposed to BPA by drinking water at doses of 1 or 10 μg/mL for 4 weeks. The mitochondrial membrane potential (δϕ), cellular ATP levels and the parameters of oxidative stress were measured in spleen cells. Measures of oxidative stress were also performed on the liver and kidneys of these hosts. The results showed a statistically significant induction of mitochondrial dysfunction, including decreased δϕ and ATP levels. Decreased activities of superoxide dismutase (SOD) and total anti-oxidative capacity (T-AOC), and increased malondialdehye (MDA) levels were also found in spleens of BPA-exposed mice. These parameters of oxidative stress were also noted in the kidneys, but only at the highest dose of BPA tested; liver parameters remained unaffected regardless of BPA dose. Data from this study demonstrate that BPA led to mitochondrial dysfunction in splenocytes and that this dysfunction was seemingly associated with an increase in local oxidative stress.