Bisphenol A impairs mitochondrial function in the liver at doses below the no observed adverse effect level.
Bisphenol A impairs mitochondrial function in the liver at doses below the no observed adverse effect level.
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DOI：
10.3346/jkms.2012.27.6.644
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发表时间：
2012-06
影响因子：
4.5
通讯作者：
Park YJ
中科院分区：
文献类型：
--
作者：
Moon MK;Kim MJ;Jung IK;Koo YD;Ann HY;Lee KJ;Kim SH;Yoon YC;Cho BJ;Park KS;Jang HC;Park YJ
据报道，双酚 A (BPA) 具有肝毒性。我们研究了这样的假设：低于未观察到的不良反应水平 (NOAEL) 的 BPA 可以通过增加肝脏的氧化应激来诱导肝损伤和线粒体功能障碍。给小鼠腹膜内注射两剂 BPA，即 0.05 和 1.2 毫克/公斤体重/天，持续 5 天。两种治疗都会损害肝线粒体的结构，尽管耗氧率和呼吸复合物的表达仅在较高剂量时下降。 BPA 处理后，肝脏中丙二醛 (MDA)（一种脂质过氧化的天然产物）水平升高，而谷胱甘肽过氧化物酶 3 (GPx3) 的表达降低。促炎细胞因子如白细胞介素6（IL-6）和肿瘤坏死因子-α（TNF-α）的表达水平也增加。在 HepG2 细胞中，10 或 100 nM BPA 还会降低耗氧率、ATP 产生和线粒体膜电位。总之，低于 NOAEL 的 BPA 剂量会引起肝脏线粒体功能障碍，这与氧化应激和炎症的增加有关。
Bisphenol A (BPA) has been reported to possess hepatic toxicity. We investigated the hypothesis that BPA, below the no observed adverse effect level (NOAEL), can induce hepatic damage and mitochondrial dysfunction by increasing oxidative stress in the liver. Two doses of BPA, 0.05 and 1.2 mg/kg body weight/day, were administered intraperitoneally for 5 days to mice. Both treatments impaired the structure of the hepatic mitochondria, although oxygen consumption rate and expression of the respiratory complex decreased only at the higher dose. The hepatic levels of malondialdehyde (MDA), a naturally occurring product of lipid peroxidation, increased, while the expression of glutathione peroxidase 3 (GPx3) decreased, after BPA treatment. The expression levels of proinflammatory cytokines such as interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) also increased. In HepG2 cells, 10 or 100 nM of BPA also decreased the oxygen consumption rate, ATP production, and the mitochondrial membrane potential. In conclusion, doses of BPA below the NOAEL induce mitochondrial dysfunction in the liver, and this is associated with an increase in oxidative stress and inflammation.
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