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目的通过线粒体孵育液染汞并用N-乙酰半胱氨酸(NAC)干预研究汞对大鼠肾皮质线粒体损伤的影响。方法提取Wistar大鼠肾皮质线粒体液并分设为阴性对照组,5、50、500μmol/L氯化汞(HgCl2)直接染毒组及线粒体液NAC预处理后50μmol/L HgCl2染毒组5组。各组于培养箱内37℃孵育1 h后,测定Na+-K+-三磷酸腺苷(ATP)酶活力、Ca2+-ATP酶活力、线粒体膜电位及孵育液中细胞色素C含量。结果与阴性对照组比较,50、500μmol/L HgCl2染毒组Na+-K+-ATP酶、Ca2+-ATP酶活力及线粒体膜电位显著降低(P<0.05),细胞色素C含量显著升高(P<0.05);与50μmol/L HgCl2染毒组比较,NAC预处理后Na+-K+-ATP酶活力及线粒体膜电位显著升高,细胞色素C含量显著降低(P<0.05)。结论汞可以剂量依赖性地诱导大鼠肾皮质线粒体损伤,NAC预处理在某种程度上能有效地预防汞所致大鼠肾皮质线粒体损伤。
Objective To investigate the effect of mercury on mitochondrial damage in rat renal cortex by using mercury in mitochondrial incubation solution and N-acetyl cysteine (NAC) intervention. Methods Wistar rat renal cortex mitochondrial fluid was extracted and divided into 5 groups (negative control group, 5, 50, 500μmol / L HgCl2 direct exposure group and mitochondrial NAC pretreatment 50μmol / L HgCl2 exposure group). After incubating at 37 ℃ for 1 h, the activities of Na + -K + -ATPase, Ca2 + -ATPase, mitochondrial membrane potential and cytochrome C in the incubation solution were determined. Results Compared with the negative control group, the activities of Na + -K + -ATPase, Ca2 + -ATPase and mitochondrial membrane potential were significantly decreased (P <0.05) and the contents of cytochrome C in 50 and 500μmol / L HgCl2 groups were significantly increased (P < 0.05). Compared with 50μmol / L HgCl2 treatment group, Na + -K + -ATPase activity and mitochondrial membrane potential were significantly increased and cytochrome C content was significantly decreased after NAC pretreatment (P <0.05). Conclusion Mercury can induce mitochondrial damage in rat renal cortex in a dose-dependent manner. Pretreatment with NAC can, to some extent, effectively prevent mitochondrial damage induced by mercury in rat renal cortex.