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目的观察丙烯酰胺染毒后小鼠心肌超微结构及心肌线粒体酶的改变,探讨丙烯酰胺的心肌毒性。方法健康清洁级昆明种雄性小鼠48只,随机分为1个正常对照组和5、30和60 mg/(kg.d)3个丙烯酰胺剂量实验组,腹腔注射染毒。10 d处死小鼠,透射电镜观察心肌超微结构变化;心电图机检测小鼠心脏电位变化;比色法检测小鼠心肌线粒体Na+-K+-ATPase、Ca2+-ATPase;ELISA法检测细胞色素氧化酶(CCO)。结果与对照组相比,各剂量实验组小鼠心室肌细胞线粒体嵴减少或消失,线粒体部分膜融合;糖原减少,肌节出现紊乱,随着染毒剂量的增加,损伤程度加剧,呈现出剂量-效应趋势。中和高剂量组和对照组相比Na+-K+-ATP酶活力明显下降(P<0.05);各实验组和对照组相比Ca2+-ATPase、CCO均下降并存在剂量依赖关系(P<0.05)。结论丙烯酰胺摄入后,可造成小鼠心肌超微结构及线粒体相关酶表达改变,提示丙烯酰胺具有心肌毒性。
Objective To observe the changes of myocardial ultrastructure and myocardial mitochondrial enzymes in mice exposed to acrylamide and to investigate the myocardial toxicity of acrylamide. Methods Forty-eight Kunming male mice were randomly divided into 1 normal control group and 3 experimental groups of acrylamide dosage of 5, 30 and 60 mg / (kg · d). The mice were injected intraperitoneally. The mice were sacrificed on day 10 and the ultrastructural changes of myocardium were observed by transmission electron microscopy. The changes of cardiac potential in mice were detected by electrocardiogram. The mitochondrial Na + -K + -ATPase and Ca2 + -ATPase in myocardium of mice were detected by colorimetry. The levels of cytochrome oxidase CCO). Results Compared with the control group, the mitochondrial ridges of the ventricular myocytes of mice in each dose group decreased or disappeared and part of the mitochondrial membrane was fused; the glycogen was decreased and the sarcomeres were disordered. With the increase of the dose, the degree of injury increased Dose-effect trends. Compared with the control group, the activity of Na + -K + -ATPase in the medium and high dose groups was significantly decreased (P <0.05). Compared with the control group, the Ca2 + -ATPase and CCO decreased in a dose-dependent manner (P <0.05) . Conclusion Acrylamide intake can cause changes of myocardial ultrastructure and mitochondria-related enzymes in mice, suggesting that acrylamide has cardiotoxicity.