Miller M J, Sandoval M
Department of Pediatrics, Albany Medical College, Albany, New York 12208, USA.
Am J Physiol. 1999 Apr;276(4):G795-9. doi: 10.1152/ajpgi.1999.276.4.G795.
Nitric oxide (NO) synthesis is markedly augmented in states of inflammation, largely due to the expression of inducible nitric oxide synthase (iNOS). Although NO has anti-inflammatory consequences under basal conditions, it remains enigmatic as to why NO displays proinflammatory characteristics in chronic inflammation. Either the anti-inflammatory actions are weak and of little consequence or, alternatively, other factors influence the role of NO in chronic inflammation. We propose that the answer to this enigma lies in the conversion of NO to other higher oxides of nitrogen (NO2, nitrogen dioxide; N2O3, dinitrogen trioxide; and ONOO-, peroxynitrite). Emerging therapeutic strategies may be independent of NO synthesis; e.g., antioxidants have no direct interaction with NO but attenuate the levels and activity of higher nitrogen oxides. Thus, whereas iNOS may be a marker for the proinflammatory actions of NO, the species that mediate tissue injury/dysfunction in inflammation are likely to be nitrogen oxides other than NO.
在炎症状态下，一氧化氮（NO）的合成显著增加，这主要归因于诱导型一氧化氮合酶（iNOS）的表达。尽管在基础条件下NO具有抗炎作用，但NO在慢性炎症中表现出促炎特性的原因仍然不明。要么是抗炎作用微弱且影响不大，要么是其他因素影响了NO在慢性炎症中的作用。我们认为，这个谜团的答案在于NO向其他更高价氮氧化物（NO2，二氧化氮；N2O3，三氧化二氮；以及ONOO-，过氧亚硝酸盐）的转化。新兴的治疗策略可能独立于NO合成；例如，抗氧化剂与NO没有直接相互作用，但能降低更高价氮氧化物的水平和活性。因此，虽然iNOS可能是NO促炎作用的一个标志物，但在炎症中介导组织损伤/功能障碍的物质可能是NO以外的氮氧化物。
