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首页> 外文期刊>Frontiers in bioscience: a journal and virtual library >Nitric oxide and oxygen metabolism in inflammatory conditions: sepsis and exposition to polluted ambients
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Nitric oxide and oxygen metabolism in inflammatory conditions: sepsis and exposition to polluted ambients

机译:炎症条件下的一氧化氮和氧代谢:败血症和暴露于污染的环境

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摘要

Nitric oxide and cytokines constitute the molecular markers and the intracellular messengers of inflammatory conditions which are derived from the activation of the NF-kappaB pathway and the transcription of proinflammatory genes. Sepsis occurs with an exacerbated inflammatory response that damages tissue mitochondria and impairs bioenergetic processes. One of the current hypotheses for the molecular mechanisms underlying the complex condition of sepsis is that enhanced NO production by mtNOS leads to excessive peroxynitrite production and protein nitration in the mitochondrial matrix, causing mitochondrial dysfunction and organ failure. The mechanism of particulate matter-health effects are believed to involve inflammation and oxidative stress. Components in particles that elicit inflammation are poorly investigated, although recent research points out to the contribution of compositional elements and particle size. Nitric oxide and reactive oxygen species appears to be involved in the inflammatory conditions associated to particulate matter inhalation.
机译:一氧化氮和细胞因子构成了炎症条件的分子标志物和细胞内信使,这些分子标志物和细胞内信使来源于NF-κB途径的激活和促炎基因的转录。脓毒症发生时,炎症反应加剧,破坏了组织的线粒体并损害了生物能过程。当前关于脓毒症复杂情况的分子机制的假设之一是,mtNOS产生NO的增加会导致线粒体基质中过亚硝酸盐的产生过多和蛋白质硝化,从而导致线粒体功能障碍和器官衰竭。据信颗粒物对健康的影响机制涉及炎症和氧化应激。尽管最近的研究指出了引起炎症的颗粒成分,但对组成成分和粒径的贡献却很少。一氧化氮和活性氧似乎参与了与吸入颗粒物有关的炎症。

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