BBP致锦鲤肝脏组织线粒体损伤的研究

发布时间：2018-03-02 19:31

本文选题：邻苯二甲酸丁基苄酯(BBP)　切入点：氧化损伤　出处：《毒理学杂志》2016年06期 　论文类型：期刊论文

【摘要】：目的以锦鲤(Cyprinuscarprio)为试验动物,研究邻苯二甲酸丁基苄酯(BBP)诱导鱼类的肝脏毒性,探讨BBP对鱼类肝脏毒性的损伤机制。方法通过急性毒性试验确定BBP实验暴露浓度(5.206、2.603和1.302 mg/L),染毒周期为28 d,解剖镜和光学显微镜下观察BBP所致肝组织的病理损伤。通过测定肝脏组织氧化损伤指标:超氧化物歧化酶(SOD)、脂质过氧化产物丙二醛(MDA)和抗氧化作用的物质谷胱甘肽(GSH),能量代谢指标:琥珀酸脱氢酶(SDH)、乳酸脱氢酶(LDH)和ATP酶(Ca~(2+)-Mg~(2+)-ATPase和Na~+-K~+-ATPase)和线粒体跨膜电位(△ψm)、线粒体通透性转换孔(PTP),对BBP诱导锦鲤肝组织线粒体损伤可能机制进行探讨。结果随着暴露浓度的增加,MDA含量显著增加,SOD和GSH显著下降,SDH,ATPase活性下降,LDH活性升高,线粒体膜电位下降,PTP开放程度增大,P0.05,差异有统计学意义。结论长期暴露于BBP可导致锦鲤的肝组织出现氧化应激,造成线粒体结构和功能发生改变。
[Abstract]:Objective to study the hepatotoxicity induced by Ding Ji benzyl phthalate (BBP) in fish with Cyprinus carprio (Cyprinus carprio). Methods the exposure concentrations of BBP to fish liver were determined by acute toxicity test. The exposure concentrations of BBP were 5.206 mg / L and 1.302 mg / L respectively. The exposure period was 28 days. The pathological damage of liver tissue induced by BBP was observed under anatomic and optical microscope. The indexes of liver oxidative damage, such as superoxide dismutase (SOD), malondialdehyde (MDA), glutathione glutathione (GSH), energy metabolism index: succinate dehydrogenase (SDH), lactate dehydrogenase (lactic dehydrogenase) and ATP were measured. The possible mechanism of mitochondrial damage induced by BBP in koi carp liver tissue was studied by using BBP and Na ~ K ~ -ATPase2 ATPase and mitochondrial transmembrane potential (蠄 MN). Results with the increase of exposure concentration, the content of malondialdehyde (MDA) in the liver tissue of koi carp was significantly increased. Sod and GSH decreased significantly. Conclusion prolonged exposure to BBP can lead to oxidative stress in the liver tissues of koi carp and change the structure and function of mitochondria.
【作者单位】：哈尔滨商业大学中药学博士后科研流动站;哈尔滨商业大学生命科学与环境科学研究中心;
【基金】：中国博士后基金项目(2013M531059) 黑龙江省博士后资助项目(LBH-Z12145) 黑龙江省青年科学基金项目(QC2012C002)
【分类号】：X171.5;X503.225

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