BBP致锦鲤肝脏组织线粒体损伤的研究

Study on the liver mitochondrial injury of carp induced by BBP

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,P<0.05,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。

Objective The carp（Cyprinuscarprio） were selected for the test,to study the liver toxicity in fish induced by phthalic acid butyl benzyl ester（BBP） and explore its toxic mechanism. Method The BBP experimental exposure concentrations（5. 206,2. 603 and1. 302 mg/L） were determined,and the exposure duration were 28 days,through the results of acute toxicity test. The damage of liver was observed under microscope and light microscope. The indexes of oxidative damage of liver[Superoxide dismutase（SOD）,malondialdehyde（MDA） and antioxidant glutathione（GSH） ],energy metabolism index[Succinate dehydrogenase（SDH）,Lactate dehydrogenase（LDH）,ATPase（Ca^2＋-Mg^2＋-ATPase and Na^＋-K^＋-ATPase） ],mitochondrial transmembrane potential（△ψm） and the mitochondrial permeability transition pore（PTP） were measured to explore the mechanism of carp liver mitochondrial damage induced by BBP. Results The results indicated that with the increase of the exposure dose,the content of MDA increased significantly,SOD and GSH content decreased significantly,the increase of LDH activity,the decline of mitochondrial membrane potential,the opening of PTP increased,All differences are statiscally significant at P〈0. 05 confidence. Conclusion The results showed that long term exposure to BBP induced oxidative stress in the liver tissues and caused mitochondrial structure and function disorder.