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目的通过亚急性汞染毒实验研究N-乙酰半胱氨酸(NAC)对汞所致大鼠肾皮质线粒体能量代谢的影响。方法将24只清洁级Wistar大鼠按体重随机分为分别为对照组、汞染毒组和NAC+汞染毒组,每组8只。对照组、汞染毒组大鼠腹腔注射生理盐水,NAC+汞染毒组腹腔注射0.480mmol/L的NAC,注射剂量为5ml/kg;2h后,对照组皮下注射生理盐水,汞染毒组和NAC+汞染毒组大鼠皮下注射368μmol/L的HgCl2溶液,注射剂量为5ml/kg。每天注射1次,连续注射14天。最后一次注射24h后,处死大鼠,取肾皮质,梯度离心得线粒体,测定丙二醛(MDA)含量、磷脂酶A2(PLA2)和琥珀酸脱氢酶(SDH)的活力以及线粒体膜电位。结果与对照组相比,汞染毒组大鼠肾皮质线粒体中MDA含量和PLA2活力以及膜电位升高,SDH活力下降,差异均有统计学意义(P<0.05,P<0.01);NAC+汞染毒组大鼠肾皮质线粒体中PLA2活力升高,差异有统计学意义(P<0.05)。与汞染毒组相比,NAC+汞染毒组大鼠肾皮质线粒体中MDA含量和PLA2活力以及膜电位降低,SDH活力升高,差异均有统计学意义(P<0.05,P<0.01)。结论汞可导致大鼠肾皮质线粒体能量代谢的障碍;NAC预处理能降低汞所致大鼠肾皮质线粒体能量代谢的障碍。
Objective To investigate the effect of NAC on energy metabolism of mitochondria in rat renal cortex induced by mercury by subacute mercury exposure. Methods Twenty-four clean-grade Wistar rats were randomly divided into control group, mercury-treated group and NAC + mercury-treated group, with 8 rats in each group. In the control group, the rats in the mercury-exposed group were intraperitoneally injected with saline and the NAC + mercury group were intraperitoneally injected with 0.480 mmol / L of NAC at a dose of 5 ml / kg. After 2 hours, the rats in the control group were injected subcutaneously with normal saline, Rats in NAC + mercury exposure group were injected subcutaneously with 368μmol / L HgCl2 solution at a dose of 5ml / kg. Injected once a day, continuous injection of 14 days. After the last injection, the rats were sacrificed, and the mitochondria were isolated from the cortex and centrifuged. The contents of malondialdehyde (MDA), phospholipase A2 (PLA2) and succinate dehydrogenase (SDH) and mitochondrial membrane potential were measured. Results Compared with the control group, the content of MDA and the activity of PLA2 in the mitochondria and the increase of membrane potential and the activity of SDH in renal cortex mitochondria in mercury-treated rats decreased significantly (P <0.05, P <0.01) The activity of PLA2 in the renal cortex mitochondria in the exposed group was significantly increased (P <0.05). Compared with the mercury-exposed group, the content of MDA and the activity of PLA2 in the mitochondria of renal cortex and the decrease of membrane potential and the activity of SDH in renal cortex mitochondria of rats exposed to NAC + mercury were significantly different (P <0.05, P <0.01). Conclusion Mercury can cause the disturbance of mitochondrial energy metabolism in rat renal cortex. Pretreatment with NAC can reduce the disorder of mitochondrial energy metabolism induced by mercury in rat renal cortex.