Evidence suggesting a role for hydroxyl radical in passive Heymann nephritis in rats.
Evidence suggesting a role for hydroxyl radical in passive Heymann nephritis in rats.
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有证据表明羟自由基在大鼠被动海曼肾炎中的作用。
DOI：
10.1152/ajprenal.1988.254.3.f337
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发表时间：
1988
期刊：
影响因子：
--
通讯作者：
Shah,SV
中科院分区：
文献类型：
--
作者：
Shah,SV
我们研究了活性氧代谢物清除剂对被动性膜性肾病Heymann肾炎模型蛋白尿的影响。被动Heymann肾炎通过单次静脉注射抗Fx 1A IgG以10 mg/100 g体重的剂量诱导。超氧化物歧化酶是超氧化物或过氧化氢酶的清除剂，可破坏过氧化氢，但对蛋白尿无影响。相比之下，二甲基硫脲（DMTU，500 mg/kg，随后125 mg/kg，ip，每天两次），一种羟自由基清除剂，显著减少蛋白尿（第5天：抗Fx 1A 53 +/- 13，n = 18;抗Fx 1A + DMTU，21 +/- 6 mg/24 h，n = 15，P <0.001）。用125 I标记的抗Fx 1A抗体进行的实验表明，DMTU不影响沉积在肾脏中的抗体量。IgG和补体沉积在肾脏中的半定量估计显示，DMTU治疗组和对照组大鼠之间没有差异。第二种羟基自由基清除剂苯甲酸钠（150 mg/kg ip，每日两次）也导致蛋白尿显著减少（第5天：抗Fx 1A 56 +/- 7，n = 9;抗Fx 1A+苯甲酸盐，14 +/- 4 mg/24 h，n = 8，P <0.01）。由于铁在生物系统中参与产生羟基自由基，我们还检查了铁螯合剂去铁胺（DFO，35 mg/天）对抗Fx 1A诱导的蛋白尿的影响。在同时用DFO处理的大鼠中，蛋白尿显著减少（第5天：抗Fx 1A 67 +/- 13，n = 15;抗Fx 1A + DFO，29 +/- 4 mg/24 h，n = 15，P小于0.01）。（250字处删节）
We examined the effect of scavengers of reactive oxygen metabolites on proteinuria in the passive Heymann nephritis model of membranous nephropathy. Passive Heymann nephritis was induced by a single intravenous injection of anti-Fx1A IgG in a dose of 10 mg/100 g body weight. Superoxide dismutase, a scavenger of superoxide or catalase which destroys hydrogen peroxide, did not affect the proteinuria. In contrast, dimethylthiourea (DMTU, 500 mg/kg followed by 125 mg/kg ip twice a day), a scavenger of hydroxyl radical, markedly reduced the proteinuria (day 5: anti-Fx1A 53 +/- 13, n = 18; anti-Fx1A + DMTU, 21 +/- 6 mg/24 h, n = 15, P less than 0.001). Experiments with 125I-labeled anti-Fx1A antibody demonstrated that DMTU did not affect the amount of antibody deposited in the kidney. Semiquantitative estimation of IgG and complement deposition in the kidney showed no differences between the DMTU-treated and control rats. A second hydroxyl radical scavenger, sodium benzoate (150 mg/kg ip twice a day), also resulted in marked reduction in proteinuria (day 5: anti-Fx1A 56 +/- 7, n = 9; anti-Fx1A + benzoate, 14 +/- 4 mg/24 h, n = 8, P less than 0.01). Because of the participation of iron in biological systems to generate hydroxyl radical, we also examined the effect of deferoxamine (DFO, 35 mg/day), an iron chelator, on the anti-Fx1A-induced proteinuria. There was a significant reduction in proteinuria in rats treated concurrently with DFO (day 5: anti-Fx1A 67 +/- 13, n = 15; anti-Fx1A + DFO, 29 +/- 4 mg/24 h, n = 15, P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)