Big Chemical Encyclopedia

Chemical substances, components, reactions, process design ...

Articles Figures Tables About

Radicals and tissue damage

Davies, K.J.A., Quintanilha, A.T., Brooks, G.A. and Packer, L. (1982). Free radicals and tissue damage produced by exercise. Biochem. Biophys. Res. Commun. 107, 1198-1205. [Pg.181]

Edwards, S. W. (1991). Regulation of neutrophil oxidant production. In Calcium, Oxygen Radicals and Tissue Damage (Duncan, J., ed.), Cambridge University Press, U.K. [Pg.184]

Willson, R. L. Free radicals and tissue damage Mechanistic evidence from radiation studies. In Biochemical Mechanisms of Liver Injury (Slater, T. F., ed.), London-New York-San Francisco, Academic Press, 1978, pp. 123-224... [Pg.25]

Hill, H. A. O. The chemistry of dioxygen and its reduction products. In Oxygen Free Radicals and Tissue Damage. Ciba Found. Symp. 65. Amsterdam-Oxford-New York Excerpta Medica, 1979, pp. 5-17... [Pg.26]

Babior, B. M. Recent studies on oxygen metabolism in human neutrophils Superoxide and chemiluminescence. In Superoxide and Superoxide Dismutases (Michelson, A. M., McCord, J. M., Fridovich, I., eds.), London-New York-San Francisco, Academic Press, 1977, pp. 271-281 McCord, J. M., Wong, K. Phagocyte-produced free radicals Roles in cytotoxicity and inflammation. In Oxygen Free Radicals and Tissue Damage, Ciba Foundation Symposium 65, Amsterdam-Oxford-New York, Excerpta Medica, 1979, pp. 343-351... [Pg.31]

Roos, D., Weening, R. S. Defects in the oxidative killing of microorganisms by phagocytic leukocytes, in Oxygen Free Radicals and Tissue Damage, (ed.) Fitzsimons, D. W., pp. 225, Amsterdam, Excerpta Medica 1979... [Pg.68]

Bielski BFIJ, Shiue GG (1979) Reaction rates of superoxide radicals with the essential amino acids. In Oxygen free radicals and tissue damage. Ciba Foundation Symposium 65, Amsterdam, pp 43-56... [Pg.186]

Ciba Foundation Symposium 65. (1979). Oxygen Free Radicals and Tissue Damage. Excerpta Medica, New York. [Pg.17]

B. H. J. Bielski and G. G. Shiue, in Oxygen Free Radicals and Tissue Damage, Cl BA Foundation Symp. 65 (new series), Excerpta Medica, Amsterdam (1979), pp. 43-48. [Pg.306]

Under normal physiological conditions, therefore, antioxidant defences in the skin are able to modulate free-radical production. The initiation of an inflammatory event has the potential for increasing ROS production to such an extent that defence systems are overwhelmed and tissue damage occurs. This event results in the production of even more toxic oxidants and the development of overt disease requiring treatment. Section 4 of this chapter will describe the role of ROS in skin inflammation. [Pg.116]

Ion pairs created by ionizing radiation eventually produce free radicals that disrupt the biochemistry of cells, break chemical bonds, and otherwise produce cell damage. Free radicals are highly reactive atoms that scavenge electrons from other atoms or molecules, causing a chain reaction that can produce cell and tissue damage. [Pg.73]

On moist skin or mucous membranes, SO2 is converted to sulfurous acid, a direct irritant. This mechanism accounts for its ability to cause inflammation, burning sensation, and tissue damage (described below) in the eyes, throat, nose, and other respiratory tissues experiencing direct contact. Bronchoconstric-tion and other related effects may be mediated by release of leukotrienes, prostaglandins, or other inflammatory factors. How SO2 causes any of the other systemic and clastogenic effects reported below is unclear. Some evidence suggests that free radicals and oxidative stress may play a role, and that metabolites of SO2 (sulfites) may be responsible for clastogenicity. [Pg.2506]

Due to the on/off phenomena and concerns about the exact role of dopamine s contribution to free radical generation and tissue damage, most practitioners use levodopa only when the symptoms of PD cause functional impairment. When levodopa levels are maintained constant by intravenous infusion, dyskinesias and fluctuations are greatly reduced, and the clinical improvement is maintained for up to several days after returning to oral levodopa dosing. A sustained-release formulation and division of the total daily dose into more frequently administered portions have been used to overcome the on/off phenomenon. [Pg.341]

Here, R usually represents the hydroxyl radical SQH. This reaction means scavenging and transformation of the extremely reactive and tissue-damaging 8DH into harmless hydroxyl ions (OH ). [Pg.343]


See other pages where Radicals and tissue damage is mentioned: [Pg.170]    [Pg.186]    [Pg.170]    [Pg.186]    [Pg.865]    [Pg.1288]    [Pg.199]    [Pg.197]    [Pg.61]    [Pg.214]    [Pg.395]    [Pg.489]    [Pg.74]    [Pg.33]    [Pg.865]    [Pg.646]    [Pg.405]    [Pg.134]    [Pg.379]    [Pg.657]    [Pg.630]    [Pg.764]    [Pg.676]    [Pg.357]    [Pg.6]    [Pg.84]    [Pg.48]   
See also in sourсe #XX -- [ Pg.14 , Pg.213 ]




SEARCH



Free radical pathways of macromolecular damage and tissue destruction - some topical examples

How do free radicals damage cells and tissues

Tissue damage

© 2024 chempedia.info