Nitric oxide and oxygen metabolism in inflammatory conditions: sepsis and exposition to polluted ambients
Nitric oxide and oxygen metabolism in inflammatory conditions: sepsis and exposition to polluted ambients
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DOI：
10.2741/2117
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发表时间：
2007-01-01
影响因子：
3.1
通讯作者：
Evelson, Pablo A.
中科院分区：
文献类型：
--
作者：
Alvarez, Silvia;Evelson, Pablo A.
一氧化氮和细胞因子构成炎症状态的分子标志物和细胞内信使，其来源是核因子-kappaB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，破坏组织线粒体，损害生物能量过程。目前对脓毒症复杂情况的分子机制的一个假说是，mtNOS增加NO的产生导致线粒体基质中过多的过氧亚硝酸盐产生和蛋白质硝化，导致线粒体功能障碍和器官衰竭。颗粒物对健康的影响机制被认为涉及炎症和氧化应激。尽管最近的研究指出了组成元素和颗粒大小的影响，但对引发炎症的颗粒中的成分研究得很少。一氧化氮和活性氧类似乎与吸入颗粒物相关的炎症状态有关。
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.