title: Taurine protects against oxidant-induced lung injury: possible mechanism(s) of action.
abstract: It is thought that oxidant-induced tissue damage is not a direct effect of the oxidant per se, but rather results from the inflammatory response that occurs thereafter. As a result of inflammation following oxidant exposure, there are neutrophils, monocytes, and macrophages with myeloperoxidase-H2O2-halide activity in the lung. Leukocytes and especially neutrophils contain high intracellular concentrations (22-50mM) of taurine (6, 8, 11, 20). Taurine acts as a trap for toxic hypochlorous acid (HOCl) and forms the less reactive metabolite, N-chlorotaurine (5-6). Thus, the biological activity of halide-dependent myeloperoxidase may be regulated by endogenous taurine. Although taurine had no effect in the present study, polymorphonuclear leukocytes have an active myeloperoxidase system capable of producing N-chlorotaurine (9, 19) and would be present at the site of inflammation in oxidant-exposed lungs. Our data suggest that taurine via N-chlorotaurine formation may protect the lung from oxidant injury, at least in part, by inhibiting production of nitrite and TNF-alpha. Moreover, lavage cells isolated from rats pretreated with taurine and exposed to O3 have a significant decrease in the production of nitrite and TNF-alpha, compared with lavage cells from rats exposed to O3 without taurine supplementation (preliminary studies). Both the concentration of taurine and the effects of N-chlorotaurine strengthen the potential impact of this chlorinated amine in vivo. N-Chlorotaurine may protect against oxidant-induced lung injury by inhibiting production of nitrite and the release of TNF-alpha which are both known to be directly linked to tissue injury.
authors.affiliation: Department of Immunology, New York State Institute for Basic Research in Developmental Disabilities, Staten Island.
authors.forename: G
authors.initials: G
authors.lastname: Schuller-Levis
authors.forename: M R
authors.initials: MR
authors.lastname: Quinn
authors.forename: C
authors.initials: C
authors.lastname: Wright
authors.forename: E
authors.initials: E
authors.lastname: Park
mesh_terms: D000594:Amino Acid Oxidoreductases / Q000037:antagonists & inhibitors; D000818:Animals; D002478:Cells, Cultured; D005260:Female; D007700:Kinetics; D008171:Lung Diseases / Q000139:chemically induced* / Q000473:pathology / Q000517:prevention & control*; D009569:Nitric Oxide / Q000096:biosynthesis; D019001:Nitric Oxide Synthase; D009573:Nitrites / Q000378:metabolism; D016877:Oxidants; D010126:Ozone; D051381:Rats; D017207:Rats, Sprague-Dawley; D013654:Taurine / Q000031:analogs & derivatives / Q000494:pharmacology*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D009573:Nitrites; D016877:Oxidants; D014409:Tumor Necrosis Factor-alpha; D013654:Taurine; D009569:Nitric Oxide; C043410:N-chlorotaurine; D010126:Ozone; D019001:Nitric Oxide Synthase; D000594:Amino Acid Oxidoreductases