Nitric oxide and oxygen metabolism in inflammatory conditions: sepsis and exposition to polluted ambients

Abstract

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.