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Titolo:
A catechol antioxidant protocatechuic acid potentiates inflammatory leukocyte-derived oxidative stress in mouse skin via a tyrosinase bioactivation pathway
Autore:
Nakamura, Y; Torikai, K; Ohigashi, H;
Indirizzi:
Kyoto Univ, Grad Sch Agr, Div Appl Life Sci, Kyoto 6068502, Japan Kyoto Univ Kyoto Japan 6068502 , Div Appl Life Sci, Kyoto 6068502, Japan
Titolo Testata:
FREE RADICAL BIOLOGY AND MEDICINE
fascicolo: 9, volume: 30, anno: 2001,
pagine: 967 - 978
SICI:
0891-5849(20010501)30:9<967:ACAPAP>2.0.ZU;2-R
Fonte:
ISI
Lingua:
ENG
Soggetto:
XANTHINE-OXIDASE INHIBITOR; ORNITHINE DECARBOXYLASE INDUCTION; ABERRANT CRYPT FOCI; PROTEIN KINASE-C; TUMOR PROMOTION; PHORBOL-ESTER; 1'-ACETOXYCHAVICOL ACETATE; CITRUS AURAPTENE; MEDIATED CYTOTOXICITY; METABOLIC-ACTIVATION;
Keywords:
phenolic antioxidant; protocatechuic acid; tyrosinase; inflammation; TPA; mouse skin; free radicals;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
51
Recensione:
Indirizzi per estratti:
Indirizzo: Ohigashi, H Kyoto Univ, Grad Sch Agr, Div Appl Life Sci, Kyoto 6068502, Japan Kyoto Univ Kyoto Japan 6068502 ife Sci, Kyoto 6068502, Japan
Citazione:
Y. Nakamura et al., "A catechol antioxidant protocatechuic acid potentiates inflammatory leukocyte-derived oxidative stress in mouse skin via a tyrosinase bioactivation pathway", FREE RAD B, 30(9), 2001, pp. 967-978

Abstract

The modifying effects of topical application of a catechol antioxidant protocatechuic acid (PA) on 12-O-tetradecanoylphorbol-13-acetate (TPA)-inducedinflammatory responses in mouse skin were investigated. Treatment with a high dose (20,000 nmol) of PA, based on time of application, modifies inflammatory responses in the skin of the B6C3F(1) mouse, a resistant strain to inflammatory response induction by TPA, but shows much higher tyrosinase expression than that of an albino mouse. The responsibility of a large amount of PA-induced leukocyte infiltration to an inflamed region in a B6C3F(1) mouse is mon sensitive than that of an ICR albino mouse. When ICR mice were treated with TPA (1.6 nmol) twice weekly for 5 weeks to induce chronic inflammatory responses, pretreatment with 1600 nmol PA 30 min prior to each TPA treatment significantly enhanced the inflammatory responses including edemaformation, leukocyte infiltration, and the level of thiobarbituric acid-reacting substances. The dose-dependency was closely parallel to the results of a tumor promotion study of PA previously reported. Further, the treatment of PA alone resulted in tyrosinase-dependent contact hypersensitivity in ICR mouse skin. In addition, the in vitro study of cytotoxicity demonstrated that bioactivation by tyrosinase but not myeloperoxidase of PA significantly enhanced cytotoxicity and intracellular glutathione consumption. We conclude that the tyrosinase-derived reactive quinone intermediate(s) of PA, which binds nucleophilic residues of proteins including sulfhydryl group andconjugates of which are recognized as haptens, was partially involved in alteration of the cellular immune functions including oxygen radical-generating leukocytes migration to inflamed regions. (C) 2001 Elsevier Science Inc.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 06/04/20 alle ore 11:08:23