锰的离子价态对大鼠心肌线粒体膜电位的影响

来源 :环境与职业医学 | 被引量 : 0次 | 上传用户:w66827552
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[目的]通过实验观察染锰后大鼠心肌线粒体膜电位(ΔΨM)的变化,探讨不同价态锰在不同剂量时,对心肌线粒体的毒作用及其强度。[方法]Wistar4月龄大鼠,断头处死,提取心肌线粒体,分别用Mn2+和Mn3+(终浓度为50、100、200、400μmol/L)染毒10min后,加入含罗丹明(Rhodamin123)的反应缓冲液中,用单波长荧光分光光度计测定在激发波长503nm、发射波长527nm条件下,3min内样品罗丹明荧光值的改变,代表ΔΨM的变化。[结果]Mn2+各染毒剂量组与对照组比较,ΔΨM下降,且差异有显著性(P<0.05);各染毒剂量组之间ΔΨM差异无显著性。Mn3+各染毒剂量组ΔΨM明显低于对照组,且差异有显著性(P<0.05)。各染锰组ΔΨM随浓度的增加而降低,组间相比差异有显著性(P<0.05)。经回归分析Mn3+、Mn2+对ΔΨM影响的b值95%可信区间分别为(-0.0493,-0.0953)和(-0.0047,-0.0479),差异也有显著性(P<0.05)。[结论]不同价态的锰均可使心肌ΔΨM降低,产生心肌毒性;Mn3+对心肌线粒体的毒性大于Mn2+,其机制有待进一步研究。 [Objective] To investigate the mitochondrial membrane potential (ΔΨM) in rat myocardium after manganese dying and to explore the toxic effects and intensities of different valence states manganese on myocardial mitochondria at different doses. [Methods] Myocardial mitochondria were isolated from the Wistar rats of the fourth month of life and were sacrificed. The mitochondria of myocardium were extracted and treated with Mn2 + and Mn3 + (final concentrations of 50, 100, 200 and 400 μmol / L) for 10 min. Rhodamine 123 Buffer, using single wavelength fluorescence spectrophotometer to determine the change of fluorescence value of rhodamine sample within 3min under excitation wavelength 503nm, emission wavelength 527nm, representing the change of ΔΨM. [Result] The ΔΨM decreased in each dose of Mn2 + group compared with the control group, and the difference was significant (P <0.05). There was no significant difference in the ΔΨM among the exposure dose groups. The ΔΨM concentrations in the Mn3 + treated groups were significantly lower than those in the control group (P <0.05). The ΔΨM decreased with the increase of the concentration of manganese in each group, the difference was significant (P <0.05). The 95% confidence intervals of b value of Mn3 +, Mn2 + on ΔΨM were (-0.0493, -0.0953) and (-0.0047, -0.0479), respectively. The difference was also significant (P <0.05). [Conclusion] Different price of manganese could decrease myocardial ΔΨM and produce cardiotoxicity. The toxicity of Mn3 + to myocardial mitochondria was greater than that of Mn2 +, and its mechanism needs further study.
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