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首页> 外文期刊>BMC Chemical Biology >Enhancement of intracellular gamma-tocopherol levels in cytokine-stimulated C3H 10T1/2 fibroblasts:relation to NO synthesis,isoprostane formation,and tocopherol oxidation
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Enhancement of intracellular gamma-tocopherol levels in cytokine-stimulated C3H 10T1/2 fibroblasts:relation to NO synthesis,isoprostane formation,and tocopherol oxidation

机译：细胞因子刺激的C3H 10T1 / 2成纤维细胞中细胞内γ-生育酚水平的增强：与NO合成，异前列腺素形成和生育酚氧化有关

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Background:Stimulation of C3H 10T1/2 murine fibroblasts with interferon-gamma (IFN)and bacterial lipopolysaccharide(LPS)generates reactive oxygen and nitrogen species leading to DNA damage, lipid oxidation,and tocopherol oxidation.The tocopherols possess unique chemical and biological properties that suggest they have important roles related to intracellular defense against radical- mediated damage. Results:Despite increased levels of reactive oxidants and decreased media tocopherol,cellular levels of gamma -tocopherol,but notα-tocopherol,were observed to increase significantly when cells were treated with IFN/LPS.Inhibition of nitric oxide(NO)synthesis by a specific inhibitor of inducible NO synthase(iNOS)increased both intracellularα-tocopherol andγ-tocopherol concentrations,but did not significantly alter the reduction in media tocopherol levels caused by IFN/LPS treatment.Both exposure to exogenous NO and cellular synthesis of NO in cell culture increased media levels of 8-epi-prostaglandin F2 alpha ,a marker of oxidative lipid damage,whereas inhibition of endogenous NO synthesis reduced media 8-epi-prostaglandin F2 alpha formation to control levels. Conclusion:Elevated intracellular levels of gamma -tocopherol in response to the cellular inflammatory state may indicate that it serves a unique role in minimizing cellular damage resulting from endogenous NO synthesis.Results of the current study suggest that NO is an important mediator of damage within the cell,as well as in the oxidation of bothα-and gamma -tocopherols.The paradoxical increase in cellular tocopherol associated with the induction of NO synthesis may indicate either enhanced cellular transport/decreased export for tocopherols or recruitment of free tocopherol from tocopherol storage molecules.
机译：背景：用干扰素-γ（IFN）和细菌脂多糖（LPS）刺激C3H 10T1 / 2鼠成纤维细胞会产生活性氧和氮，导致DNA损伤，脂质氧化和生育酚氧化。生育酚具有独特的化学和生物学特性提示它们在细胞内防御自由基介导的损伤方面具有重要作用。结果：尽管用IFN / LPS处理细胞，尽管反应性氧化剂的含量增加而培养基中的生育酚减少，但γ-生育酚而不是α-生育酚的细胞水平显着增加。通过特异性抑制剂抑制一氧化氮的合成诱导型一氧化氮合酶（iNOS）抑制剂增加细胞内α-生育酚和γ-生育酚的浓度，但并没有显着改变由IFN / LPS处理引起的介质生育酚水平的降低。细胞培养中暴露于外源NO和细胞中NO的合成均增加培养基8-前列腺素F2α的水平是氧化脂质损伤的标志，而内源性NO合成的抑制将培养基8-前列腺素F2α的形成减少到控制水平。结论：γ-生育酚的细胞内水平升高对细胞炎症状态的响应可能表明它在最小化内源性NO合成引起的细胞损伤中发挥了独特作用。目前的研究结果表明，NO是内源性NO损伤的重要介质。细胞生育酚与一氧化氮合成的诱导反常增加可能表明细胞转运/生育酚输出减少或从生育酚储存分子中募集了游离生育酚。

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