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汞对大鼠肾皮质线粒体ATP酶和膜电位的影响 被引量:8

Effects of mercury on ATPase and mitochondrial membrane potential in rat renal cortex
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摘要 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 elucidate the effects of HgCl2 exposure on mitochondria in rat renal cortex and the preventive effects of N-acetylcysteine (NAC) in vitro. Methods Mitochondria from renal cortex were prepared and divided into 5 groups : a control group ,5,50,500 μmol/L HgCl2 groups and a NAC pretreated-50 μmol/L HgCl2 group. All the groups were incubated at 37℃ for one hour. The activities of Na+ -K + -ATPase and Ca2 + -ATPase, mitoehondrial membrane potential and the content of mitochondrial cytoehrome C were detected. Results Compared with the control group, the activity of ATPase and mitochondrial membrane potential in 50 and 500 μmol/L HgCl2 groups were decreased (P 〈 0. 05 ) , the content of mitochondrial cytochreme C was increased ( P 〈 0. 05 ). While compared with 50 μmol/L HgC12 group, in the NAC pretreated group, the activity of Na+ -K+ - ATPase and the mitochandrial membrane potential were increased ( P 〈 0.05 ) , the content of mitochondrial cytochrome C was decreased ( P 〈 0. 05 ). Conclusion HgCl2 could dose-dependently induce the damage of mitochondria from renal cortex in rats ; this change could be prevented by pre-treating with NAC to some extent.
出处 《中国职业医学》 CAS 北大核心 2009年第6期461-463,共3页 China Occupational Medicine
关键词 N-乙酰半胱氨酸 线粒体膜电位 Mercury N-acetylcysteine Mitochondrial membrane potential
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  • 1李毅敏,赵树仪.N-乙酰半胱氨酸的研究进展[J].天津药学,2003,15(2):50-53. 被引量:43
  • 2SANTOS A C,UYEMURA S A,SANTOS N A,et al. Hg(Ⅱ)-induced renal cytotoxicity : in vitro and in vivo implications for the bioenergetie and oxidative status of mitochondria [ J]. Mol Cell Biochem, 1997, 177(1/2) :53 -59.
  • 3陈传义,彭仁琇,李元涛.七氟醚麻醉对大鼠脑ATP酶的动态影响[J].中华实验外科杂志,2004,21(8):972-974. 被引量:19
  • 4EMAUS R K,GRUNWALD R, LEMASTER J J. Rhodamine123 as a probe of transmembrane potential in isolated rat-liver mitochondria: spectral and metabolic properties [ J]. Biochim Biophys Acta, 1986, 850 (3) :436 - 448.
  • 5LOWRY O H, ROSEBROUGH N J, FARR A L, et al. Protein measurement with the Folin phenol reagent [ J ]. J Biol Chem, 1951, 193 ( 1 ) :265 - 275.
  • 6TRUMP B J, BEREZESDY C R. Calcium-mediated cell injury and cell death [ J]. FAEB J, 1995,9:219 -224.
  • 7IMESCH E, MOOSMAYER M,ANNER B M. Mercury weakens membrane anchoring of Na^+ -K^+ -ATPase [ J]. Am J Physiol, 1992,262 (5 Pt 2) : F837 - 842.
  • 8MURIEL P, PEREZ-ROJAS J M. Nitric oxide inhibits mitochondrial monoamine oxidase activity and decreases outer mitechondria membrane fluidity [ J ]. Comp Biochem Physiol C Toxicol Pharmacol, 2003,136(3) :191 -197.
  • 9KRICK S, PLATOSHYN O, MCDANIEI S S,et al. Augmented K^+ currents and mitochondrial membrane depolarization in pulmonary artery myocyte apoptosis [ J ]. Am J Physiol Lung Cell Mol Physiol, 2001,281 (4) :L887 - L894.
  • 10JUHASZOVA M ,ZOROV D B ,KIM S H ,et al. Glycogen synthase kinase-3beta mediates convergence of protection signaling to inhibit the mitochondrial permeability transition pore [ J ]. J Clin Invest, 2004, 113(11) :1535 -1549.

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