Glomerular arachidonate lipoxygenation in rat nephrotoxic serum nephritis.
Glomerular arachidonate lipoxygenation in rat nephrotoxic serum nephritis.
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大鼠肾毒性血清肾炎的肾小球花生四烯酸脂氧合。
DOI：
10.1172/jci112110
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发表时间：
1985
期刊：
影响因子：
--
通讯作者：
Dunn,MJ
中科院分区：
文献类型：
--
作者：
Lianos,EA;Rahman,MA;Dunn,MJ
在大鼠肾毒性血清肾炎（NSN）模型上研究了花生四烯酸脂氧合生成单羟基化二十碳四烯酸（HETE）。与对照组相比，单次输注肾毒性血清可增强肾炎大鼠肾小球中[3 H]花生四烯酸（[3 H]C20：4）向[3 H]12-HETE的转化。诱导疾病后2天，对照肾小球中[3 H]花生四烯酸的转化率为1.95 +/- 0.2%，肾炎肾小球中为14.2 +/- 2%。未观察到[3 H]C20：4转化为[3 H]5-、8-和9-HETE的显著变化。通过碱性水解提取肾小球HETE，以评价HETE产生后可能的再酰化，证实了12-HETE的存在，但未提供5-HETE合成的证据。高压液相色谱-紫外检测和12-HETE放射免疫测定也证实了肾炎大鼠肾小球12-HETE合成增加。增强肾小球12-HETE合成开始早在3-5小时后，肾毒血清给药，并在第2天达到高峰，12-HETE生产的10倍增强。肾小球12-HETE的增加持续到第7天，并在第14天恢复到对照水平。抗血小板抗血清诱导的血小板耗竭并没有减少NSN中肾小球12-HETE的合成，从而消除了血小板作为12-HETE的细胞来源。肾小球上皮细胞和系膜细胞是12-脂氧合酶活性增强的最可能来源。由于12-HETE对白细胞功能有重要作用，因此，在肾小球免疫损伤中花生四烯酸12-脂氧合的增强可能在肾小球肾炎的演变中具有重要的促炎作用。
Arachidonate lipoxygenation to monohydroxylated eicosatetraenoic acids (HETE) was studied in rat nephrotoxic serum nephritis (NSN). A single infusion of nephrotoxic serum enhanced conversion of [3H]arachidonic acid ([3H]C20:4) to [3H]12-HETE in glomeruli isolated from nephritic rats compared with controls. The percent conversion of [3H]arachidonic acid was 1.95 +/- 0.2% in control glomeruli and 14.2 +/- 2% in nephritic glomeruli 2 d after induction of disease. No significant changes in the conversion of [3H]C20:4 to [3H]5-, 8-, and 9-HETE were noted. Extraction of glomerular HETE by alkaline hydrolysis, to evaluate possible reacylation of HETE after their production, confirmed the presence of 12-HETE and did not provide evidence of 5-HETE synthesis. Increased glomerular 12-HETE synthesis in nephritic rats was also demonstrated by high pressure liquid chromatography-UV detection and by 12-HETE radioimmunoassay. The enhanced glomerular 12-HETE synthesis commenced as early as 3-5 h after administration of nephrotoxic serum and peaked at day 2 with 10-fold enhancement of 12-HETE production. Increments of glomerular 12-HETE persisted on day 7 and returned toward control levels by day 14. Platelet depletion, induced by antiplatelet antisera, did not decrease glomerular 12-HETE synthesis in NSN, thereby eliminating platelets as the cellular origin of 12-HETE. Glomerular epithelial and mesangial cells are the most likely sources of enhanced 12-lipoxygenase activity. The enhanced arachidonate 12-lipoxygenation in glomerular immune injury could have important proinflammatory effects in the evolution of glomerulonephritis since 12-HETE has important effects on leukocyte function.
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发表时间：
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Virchows Archiv B Cell Pathology Including Molecular Pathology
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