Free radicals in lung

B46. Brigham, K. L., Role of free radicals in lung injury. Chest 89,859-863 (1986). 

Ethane, a simple hydrocarbon, C2H6, seems to be formed by the unusually high concentration of free radicals in patients with a tendency to cancerous growths. These radicals attack proteins and make hydrocarbons, including ethane. A gas detector is being tested to see if the presence of ethane in the breath can be used to detect lung cancer in patients who have shown symptoms.3... 

C. Doeleman and A. Bast, Oxygen Radicals in Lung Pathology. Free Rad Biol. Med 9 (1990) 381-340. 

Ascorbic acid reacts with 02" generated from the xanthine oxidase system and may play a role against 02" mediated toxicity. Ascorbic acid quenches the hydroxyl radical (40), Ascorbic acid may protect against free radicals in the lung because ascorbic acid is found in the fluid (39). The toxicity of ozone and oxygen may also be reduced by ascorbic acid (39). Carbon tetrachloride mortality in rats is lowered by ascorbic acid. Autoxidation of ascorbic acid did not generate 02". Reduced glutathione reacts with dehydroascorbic acid (VII) and recycles ascorbic acid. 

In the lung, the alveolar type I cell is directly exposed to these oxidants in the atmosphere and in tobacco smoke. It is also exposed to oxidants in the blood that diffuse through the blood-air barrier. While the resistance of this cell against oxidants is very low, it also constitutes 95% of the alveolar surface area exposed to the inhaled air (Naimark, 1977). The cell membrane of the type I cell is therefore a relatively large target for free radicals in the inhaled air and is very susceptible to peroxidation of the lipids in its membranes. The cell plasma membrane is a critical site of free radical reactions for several reasons. Extracellularly generated free radicals must cross the... 

Ozone, O3, has several toxic effects. At 1 ppm by volume in air, ozone causes severe irritation and headache and irritates the eyes, upper respiratory system, and lungs. Inhalation of ozone can sometimes cause fatal pulmonary edema (abnormal accumulation of fluid in lung tissue). Ozone generates free radicals in tissue that can cause lipid peroxidation, oxidation of sulfhydryl (-SH) groups, and other destructive oxidation processes. 

Alpha-l-antiprotease (ai-AP) limits tissue damage arising from the actions of the leucocyte protease, elastase (Carrell and Travis, 1985), and there is much evidence available for the oxidative inactivation of this protein by oxygen-derived free-radical species and hypochlorous acid/hypochlorite anion (HOCl/OCP). The mechanism of this inactivation appears to involve the oxidation of a critical methionine residue (Met-358) to its corresponding sulphoxide and methionine sulphoxide has been detected in ai-AP samples isolated from the lungs of cigarette smokers (Carp et al., 1982) and rheumatoid synovial fluids (Wong and Travis, 1980). 

Smith, L.J., Houston, M. and Anderson, J. (1993). Increased levels of glutathione in bronchoalveolar lavage fluid from patients with asthma. Am. Rev. Resp. Dis. 147, 1461-1464. Smith, L.L. (1986). The response of the lung to foreign compounds that produce free radicals. Ann. Rev. Physiol. 48, 681-692. 

Evans, P.H., Campbell, A.K., Yano, E. and Goodman, B. (1987). Phagocytic oxidant stress and antioxidant interactions in the pneumoconioses and dust-induced tumourigenic lung disease. In Free Radicals, Oxidant Stress and Drug Action (ed. C. Rice-Evans) pp. 213-235. Richelieu, London. 

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