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目的探讨氟化物对离体培养大鼠心肌细胞的毒性作用机制。方法应用离体培养心肌细胞模型和细胞化学方法研究不同剂量的氟化钠处理后,细胞搏动或停搏与心肌细胞内糖原的水平及琥珀酸脱氢酶(SDH)活力的变化。结果心肌细胞的停搏率与氟离子(F-)剂量间存在明显的正相关关系(r=0.969、P<0.05),F-的半数停搏物质的量浓度为1.92×10-4mol/L。细胞化学研究及图像分析数据表明,对照组心肌细胞内糖原和SDH反应都呈强阳性,实验组停搏的心肌细胞这2种反应随着F-剂量增加而减弱,呈负相关关系(r分别为-0.917 3,-0.960 3),且不同剂量组间差异都有统计学意义(P<0.05)。结论氟化钠可使心肌细胞内糖原的合成受阻及SDH活力被抑制,导致搏动的心肌细胞因能量供应不足而停搏,呈明显的剂量-反应关系。
Objective To investigate the toxic mechanism of fluoride on cultured rat cardiomyocytes. Methods The in vitro cultured cardiomyocyte model and cytochemical method were used to investigate the changes of cardiomyocyte glycogen level and the activity of succinate dehydrogenase (SDH) after cardioversion or cardioplegia with different doses of sodium fluoride. Results There was a significant positive correlation between cardiomyocyte arrest rate and fluoride ion (F-) dose (r = 0.969, P <0.05). The F-half-arrest substance concentration was 1.92 × 10-4 mol / L . Cytochemistry and image analysis data showed that the glycogen and SDH responses in the control group were all strongly positive. The two responses of the cardiomyocytes in the experimental group weakened with the increase of the F-dose, with a negative correlation (r Respectively, -0.917 3, -0.960 3), and the differences between different dose groups were statistically significant (P <0.05). Conclusion Sodium fluoride inhibited the synthesis of glycogen and inhibited the activity of SDH in cardiomyocytes, resulting in a pulsatile cardiomyocyte arrest due to insufficient energy supply. It showed a dose-response relationship.