羧乙基锗倍半氧化物对正常和异丙基肾上腺素损伤培养乳鼠心肌细胞的影响

羧乙基锗倍半氧化物(Ge—132)能促进培养乳鼠心肌细胞DNA和RNA的合成,提高超氧化物歧化酶(SOD)的活性,维持细胞膜结构的稳定。异丙基肾上腺素可使心肌细胞乳酸脱氢酶(LDH)释放增加,细胞搏动停止,超微结构显示肌膜和线粒体严重受损。Ge—132可显著减少异两基肾上腺素引起心肌细胞释放LDH,维持细胞的搏动功能和超微结构的完整。

EFFECT OF CARBOXYETHYLGERMANIUM SESQUIOXIDE ON CULTURED NORMAL NEONATAL RAT MYOCARDIAL CELLSAND CELLS INJURED BY ISOPROTERENOL

The effect of carboxyethylgermanium sesquioxide (Ge-132) on culturedneonatal rat myocytes and isoproterenol injured myocytes was studied. The results showedthat Ge-132 (0. 01 mmnol.L~(-1)and 1 mmol.L~(-1)) increased the incorporation of both [3~H]-TdR and [(14)~C]-UR, reduced the membrane lipid fluidity and inhibital the release of thecytoplasmic enzyme lactate dehydrogenase (LDH). Exposure of the myocytes toisoproterenol 0.5 mmol.L~(-1) for 6 hours resultal in 5-fold release of LDH comparedwith the control. All myocytes ceased beating. Ultrastucturally, severe sarcolemmal andmitochondrial damage was evident. When the cells were pretreated with Ge-132 beforethe addition of isoperterenol, the increased LDH release was idhibital significantly, andpreservation of beat and ultrastructure of myocytes was observed. In addition, the activityof superoxide dismutase (SOD) was elevated by Ge-132. All the effects of Ge-132 weredose-reated. The results indicate that Ge-132 may improve the metabolism of culturedneonatal rat myocytes and protect myocytes from isoproternol-induced injury.