N-乙酰半胱氨酸对汞致大鼠肾皮质线粒体能量代谢损伤的影响

Antagonism of N-acetylcysteine to Energy Metabolism Damage of Renal Cortical Mitochondria Induced by Mercury in Rats

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 explore the effect of HgC12 exposure on energy metabolism of renal mitochondria in rats and the preventive effect of N-acetylcysteine （NAC）. Methods Twenty-four Wistar rats were randomly divided into control group, HgCl2 group and NAC ＋HgCl2 group by body weight, 8 in each. Control group and HgCl2 group were treated with physiological saline through intraperitoneal injection, NAC＋HgCl2 group rats were intraperitoneally pretreated with NAC （0.4 mmol/kg）, two hours after treatment,HgCl2 group and NAC＋HgCl group were injected subcutaneously with HgCl2 （1.84 μ mol/kg）,but control group was injected with physiological saline, the volume of was 5 ml]kg, once a day for 14 consecutive days. Twenty-four hours after the last injection, all rats were sacrificed and the cortices of rat kidneys were collected. The mitochondria were prepared by using the differential centrifugation. The levels of malondialdehyde （MDA）,the activities of phospholipase A2 （PLA2） and succinate dehydrogenase （SDH）,the mitoebondrial membrane potential were measured. Results Compared with control group,the level of MDA and the activity of PLA2 significantly increased in HgCl2 group （P 〈0.01） , the activity of SDH and mitoehondrial membrane potential significantly decreased （P〈0.05） in HgC12 group. Compared with HgCl2 group,the level of MDA and the activity of PLA2 significantly decreased （P〈0.05 ,P〈0.01）, the activity of SDH and mitochondrial membrane potential significantly increased （P〈0.05） in NAC＋HgC12 group. Conclusion Mercury may induce the decline of energy metabolism in the mitochondria of rat renal cortices, and the pre-treatment of NAC can reduce the effect of mercury.