铁增强了二硫代氨基甲酸盐对脓毒性休克小鼠组织中一氧化氮的清除作用。
Iron potentiates nitric oxide scavenging by dithiocarbamates in tissue of septic shock mice.
作者信息
Komarov A M, Mak I T, Weglicki W B
机构信息
Department of Medicine, The George Washington University Medical Center, Washington, DC 20037, USA.
出版信息
Biochim Biophys Acta. 1997 Oct 24;1361(3):229-34. doi: 10.1016/s0925-4439(97)84636-4.
Vanin and co-workers (Kubrina et al., Biochim. Biophys. Acta 1176 (1993) 240-244; Mikoyan et al., Biochim. Biophys. Acta 1269 (1995) 19-24) reported that short term (30 min) iron (Fe) exposure potentiates nitric oxide (NO) production in tissues of septic shock mice, based on increased formation of NO complex by diethyldithiocarbamate (DETC). We have reexamined the effect of Fe administration in mice treated with Escherichia coli lipopolysaccharide (LPS) and have not found any changes in nitrosylhemoglobin (HbNO) or (NOs- + NO3-) levels in blood 30 min after Fe-citrate complex injection. However, Fe-citrate promotes NO complex formation by iron-dependent NO traps: DETC, pyrrolidinedithiocarbamate (PDTC) and N-methyl-D-glucamine dithiocarbamate (MGD), when given simultaneously at 6 h after LPS. Rather than potentiation of NO production, our data support that short-term iron treatment (30 min) enhances in vivo spin trapping ability of dithiocarbamate.
瓦宁及其同事（库布丽娜等人，《生物化学与生物物理学报》1176卷（1993年）240 - 244页；米科扬等人，《生物化学与生物物理学报》1269卷（1995年）19 - 24页）报道，基于二乙基二硫代氨基甲酸盐（DETC）使一氧化氮（NO）复合物形成增加，短期（30分钟）铁（Fe）暴露可增强脓毒症休克小鼠组织中NO的生成。我们重新研究了给用大肠杆菌脂多糖（LPS）处理的小鼠施用铁的效果，在注射柠檬酸铁复合物30分钟后，未发现血液中亚硝基血红蛋白（HbNO）或（NO₂⁻ + NO₃⁻）水平有任何变化。然而，柠檬酸铁在LPS处理6小时后同时给予时，可通过铁依赖性NO捕获剂促进NO复合物形成：DETC、吡咯烷二硫代氨基甲酸盐（PDTC）和N - 甲基 - D - 葡糖胺二硫代氨基甲酸盐（MGD）。我们的数据支持短期铁处理（30分钟）增强了二硫代氨基甲酸盐的体内自旋捕获能力，而非增强NO的生成。
Zotero 插件