Dutta Mousumi, Paul Goutam
Molecular Neurotoxicology Laboratory, Department of Physiology, University of Kalyani, Kalyani, Nadia, 741235, West Bengal, India.
Toxicol Rep. 2019 Jun 17;6:578-589. doi: 10.1016/j.toxrep.2019.06.011. eCollection 2019.
Humans are often exposed to bisphenol A (BPA), the monomer of polycarbonate plastics and epoxy resins, through BPA contaminated drinking water, beverages and foods, packaged in polycarbonate plastic bottles and cans coated with epoxy resins due to leaching. Several research groups have reported that BPA may cause damage of mitochondria in liver, kidney, heart and brain cells by inducing oxidative stress. The antioxidant efficacy of gallic acid (GA), a polyphenol compound obtained from plants, against different toxicants induced oxidative stress has been well established. The aim of the present study was to examine the protective efficacy of GA against BPA induced oxidative damages of the rat liver mitochondria . In our study, we have found a significant decrease in the intactness of mitochondria; a significant increase () in the levels of lipid peroxidation end product (i.e. malondialdehyde) and protein carbonylation product; and also a significant decrease () in the reduced glutathione content; when mitochondria were incubated with BPA (160 μM/ml) only. These results indicate that BPA probably causes damage to the cellular macromolecules through oxidative stress. We have observed significant counteractions () against BPA induced alterations in mitochondrial intactness, lipid peroxidation and protein carbonylation products formation and reduced glutathione content when mitochondria were incubated with BPA and GA (20 μg/ml/ 40 μg/ml/ 80 μg/ml) in combination in a dose-dependent manner. Gallic acid also showed significant restorations () of the activities of antioxidant enzymes, Krebs cycle enzymes, respiratory chain enzymes and thiolase when mitochondria were incubated with BPA and dosage of GA (20 μg/ml/ 40 μg/ml/ 80 μg/ml) in combination compared to BPA incubated mitochondria. Furthermore, GA significantly () counteracted the BPA induced decrease in tryptophan and NADH auto-fluroscence levels in mitochondria. This result suggests that GA protects the mitochondria probably by reducing the oxidative stress. Besides, GA protects the mitochondrial surface from BPA induced oxidative damages as viewed under the scanning electron microscope. Considering all the results, it can be concluded that GA shows potent efficacy in protecting the rat liver mitochondria from BPA induced oxidative stress mediated damages.
人类常常通过受双酚A（BPA）污染的饮用水、饮料和食品接触到双酚A，双酚A是聚碳酸酯塑料和环氧树脂的单体，由于其会从用环氧树脂涂层的聚碳酸酯塑料瓶和罐中渗出。几个研究小组报告称，双酚A可能通过诱导氧化应激对肝脏、肾脏、心脏和脑细胞中的线粒体造成损害。没食子酸（GA）是一种从植物中提取的多酚化合物，其对不同毒物诱导的氧化应激的抗氧化功效已得到充分证实。本研究的目的是检验没食子酸对双酚A诱导的大鼠肝脏线粒体氧化损伤的保护功效。在我们的研究中，我们发现当线粒体仅与双酚A（160μM/ml）孵育时，线粒体的完整性显著降低；脂质过氧化终产物（即丙二醛）和蛋白质羰基化产物的水平显著升高（）；还原型谷胱甘肽含量也显著降低（）。这些结果表明，双酚A可能通过氧化应激对细胞大分子造成损害。当线粒体与双酚A和没食子酸（20μg/ml/40μg/ml/80μg/ml）联合孵育时，我们观察到没食子酸以剂量依赖的方式对双酚A诱导的线粒体完整性、脂质过氧化和蛋白质羰基化产物形成以及还原型谷胱甘肽含量的改变有显著的对抗作用（）。与仅用双酚A孵育的线粒体相比，当线粒体与双酚A和不同剂量的没食子酸（20μg/ml/40μg/ml/80μg/ml）联合孵育时，没食子酸还显著（）恢复了抗氧化酶、三羧酸循环酶、呼吸链酶和硫解酶的活性。此外，没食子酸显著（）对抗了双酚A诱导的线粒体中色氨酸和NADH自发荧光水平的降低。这一结果表明，没食子酸可能通过减轻氧化应激来保护线粒体。此外，从扫描电子显微镜观察可知，没食子酸保护线粒体表面免受双酚A诱导的氧化损伤。综合所有结果，可以得出结论，没食子酸在保护大鼠肝脏线粒体免受双酚A诱导 的氧化应激介导的损伤方面显示出强大的功效。
