摘要
用含80%的 DMEM 培养基加20%小牛血清培养新生 wistar 大鼠心室肌细胞。向培养基中加入0.42×10^(-3)M 黄嘌呤与5.3×10^(-8)M 黄嘌呤氧化酶,使心肌细胞的自由基含量增高;心肌细胞动作电位 APA、OS、MDP、TP、Vmax、APD_(90)等均减小;心肌细胞输入阻抗降低;并呈现以肌丝、线粒体损伤为主的心肌细胞超微结构改变。向培养基中添加0.1ppm Mn,可以抵销黄嘌呤—黄嘌呤氧化酶(X—XOD)对细胞的损伤作用。这可能是 X—XOD 诱发(?)导致心肌细胞的自由基损伤,而 Mn 通过 SOD 实现其清除自由基作用,从而对抗心肌细胞的自由基损伤。
The cultured cardiac cells from ventricular of neogenesis Wistar white rat wereused to 80% DMEM medium added 20% calf serum.The medium had added0.4X10^(-3)M xanthine(X)and 5.3X 10^(-8M)M xanthine oxidase(XOD),so that the freeradical has been increase in cultured cardiac cells,and the membrane of cardiaccells,had appeared injury state.Right now,the parameter of acting potentialhad the reduction which are Acting Potential Amplitude(APA),Over shoot(OS),Maximal Diastolic Potential(MDP),Threshold Potential(TP),Maximal Depolarization Voltage(Vmax),Acting Potential Duration Per 90(APD90),Afferent Impedance(AIP).In addition,the myofilament and mitochodrion had happened injury state fromultrastructure of medium added 0.1PPm manganese(Mn),the effects of X-XODhad resisted on injury action of cardiac cells.The X-XOD had induced injury effect of free redical of on cardiac cells,TheMn had passed Superoxide Dismutase(SOD)of getrid of free radical and resis-ted the effect of free redical on cardiac cells.
出处
《中国地方病学杂志》
CAS
CSCD
1990年第5期272-277,共6页
Chinese Jouranl of Endemiology
关键词
锰
心肌细胞培养
抗氧化作用
Xanthine
Xanthine Oxidase
Free radical
Action Potential
