A. Pappa, R. Franco, O. Schoneveld, A. Galanis, R. Sandaltzopoulos, M. I. Panayiotidis, A. Pappa, R. Franco, O. Schoneveld, A. Galanis, R. Sandaltzopoulos and M. I. Panayiotidis Pages 2590 - 2596 ( 7 )
Over 95% of the oxygen we metabolize undergoes a four-electron reduction to produce two molecules of water. Whenever electrons escape from the mitochondrial electron-transport chain and pass directly onto oxygen, oxidants that can cause cytotoxicity are generated. The lung being constantly exposed to atmospheric oxygen is more susceptible to oxidant-induced cellular damage. For instance, increased generation of oxidants is implicated in many pulmonary pathological conditions including emphysema, adult respiratory distress syndrome, idiopathic pulmonary fibrosis and asthma. Sulfur is an essential major inorganic element with a recently described protective cellular role. One of its many biologically important functions is the formation of disulfide bridges between two cysteine molecules thus stabilizing protein conformation. Also, it provides the site for attachment and transfer of 1-C methyl groups via formation of S-adenosylmethionine, and most importantly it is an essential constituent of the antioxidant tripeptide, glutathione, and vitamins like thiamin and biotin. However, its protective role emanates from its antioxidant properties in the context of sulfur-containing compounds (S-adenosylmethionine, cysteine, taurine, glutathione etc) that are known to act in protecting against oxidant-induced lung disease. The efficacy of these sulfur-containing compounds in scavenging oxidants directly or indirectly and consequently protecting against lung diseases is discussed herein.
Lung diseases,oxidants,antioxidants,oxidative stress,cellular toxicity,sulfur-containing compounds,sulfur metabolism,glutathione
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