Bisphenol A impairs mitochondrial function in spleens of mice via oxidative stress
Bisphenol A impairs mitochondrial function in spleens of mice via oxidative stress
复制标题
双酚 A 通过氧化应激损害小鼠脾脏的线粒体功能
DOI：
10.1007/s13273-013-0049-5
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发表时间：
2013-12-01
影响因子：
1.7
通讯作者：
Wang, Xiaofei
中科院分区：
文献类型：
--
作者：
Dong, Youdan;Zhai, Lingling;Wang, Xiaofei
越来越多的证据表明，双酚A（BPA）影响免疫反应，其机制主要被认为是对多种免疫细胞的雌激素效应。BPA除了具有雌激素活性外，还可导致肝脏、肾脏和大脑的氧化损伤。由于有关BPA对脾脏（引发原发性免疫应答的主要部位）影响的信息有限，尤其是没有关于其对脾脏线粒体功能作用的数据。为了评估这种影响，C57 BL/6雌性小鼠通过饮用1或10 μg/mL剂量的BPA持续4周。测定脾细胞线粒体膜电位（δ ε）、细胞ATP水平和氧化应激参数。还对这些宿主的肝脏和肾脏进行了氧化应激的测量。结果显示，线粒体功能障碍的诱导具有统计学显著性，包括δ ε和ATP水平降低。BPA染毒小鼠脾脏超氧化物歧化酶（SOD）活性和总抗氧化能力（T-AOC）降低，丙二醛（MDA）含量升高。在肾脏中也观察到这些氧化应激参数，但仅在测试的最高剂量BPA下;无论BPA剂量如何，肝脏参数均不受影响。这项研究的数据表明，BPA导致脾细胞线粒体功能障碍，这种功能障碍似乎与局部氧化应激的增加有关。
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.