Trace element levels in the experimental peritonitis

Dildar Konukoğlu, Meltem Ercan, Erkal Ziylan
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Abstract

Electron transfer from iron or copper ions to oxygen is an important example of cellular free radical initiation. Oxygen-derived free radicals have been implicated as mediators of cellular injury in several model systems. To evaluate the importance of iron, copper, and zinc levels on lipid peroxidation in peritonitis, we measured peritoneum malondialdehyde (MDA) as a marker of lipid peroxidation, zinc, copper, and iron levels during an animal model of intraperitoneal sepsis. Additionally, the effects of free radical scavenger alpha-tocopherol administration were studied. The peritoneum MDA, iron, copper, and zinc levels were increased after induction of peritonitis with Escherichia coli. The treatment with alpha-tocopherol decreased peritoneum MDA, iron, and copper levels significantly but not the zinc levels. Additionally, the treatment with alpha-tocopherol 3 days prior to injection of E. coli decreased MDA, copper, and iron levels more than treatment with alpha-tocopherol at the time of injection of E. coli. Our results indicate that copper, iron, and zinc have important effects on peroxidation events in E. coli-induced peritonitis and that alpha-tocopherol treatment can improve the oxidant status. J. Trace Elem. Exp. Med. 15:79–84, 2002. © 2002 Wiley-Liss, Inc.
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实验性腹膜炎的微量元素水平
从铁或铜离子到氧的电子转移是细胞自由基引发的一个重要例子。在几个模型系统中,氧衍生的自由基被认为是细胞损伤的介质。为了评估铁、铜和锌水平对腹膜炎脂质过氧化的重要性,我们在腹膜内败血症动物模型中测量了作为脂质过氧化标志的腹膜丙二醛(MDA)、锌、铜和铁水平。此外,还研究了自由基清除剂α-生育酚给药的效果。用大肠杆菌诱导腹膜炎后,腹膜MDA、铁、铜和锌水平升高。α-生育酚治疗显著降低腹膜MDA、铁和铜水平,但不降低锌水平。此外,与注射大肠杆菌时用α-生育酚处理相比,在注射大肠杆菌前3天用α-生育醇处理更能降低MDA、铜和铁水平。我们的研究结果表明,铜、铁和锌对大肠杆菌诱导的腹膜炎的过氧化事件有重要影响,α-生育酚处理可以改善氧化状态。J.Trace Elem。Exp.Med.15:79-842002。©2002 Wiley-Liss,股份有限公司。
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International Society For Trace Element Research In Humans (ISTERH) Seventh International Conference, Bangkok, Thailand, November 7–12, 2004 Response† Erratum Fluoride: A toxic or therapeutic agent in the treatment of osteoporosis? Interleukin-1α, tumor necrosis factor-α, and interleukin-12 secreted by zinc-induced murine macrophages in vivo and in vitro
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