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Titolo:
Role of macrophages and inflammatory mediators in chemically induced toxicity
Autore:
Laskin, DL; Laskin, JD;
Indirizzi:
Rutgers State Univ, Environm & Occupat Hlth Sci Inst, Piscataway, NJ 08854USA Rutgers State Univ Piscataway NJ USA 08854 Inst, Piscataway, NJ 08854USA Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Piscataway, NJ 08854 USA Univ Med & Dent New Jersey Piscataway NJ USA 08854 scataway, NJ 08854 USA
Titolo Testata:
TOXICOLOGY
fascicolo: 1-3, volume: 160, anno: 2001,
pagine: 111 - 118
SICI:
0300-483X(20010307)160:1-3<111:ROMAIM>2.0.ZU;2-R
Fonte:
ISI
Lingua:
ENG
Soggetto:
NITRIC-OXIDE SYNTHASE; TUMOR-NECROSIS-FACTOR; ACETAMINOPHEN HEPATOTOXICITY; ACTIVATED MACROPHAGES; ENHANCED PRODUCTION; PULMONARY IRRITANT; POTENTIAL ROLE; FACTOR-ALPHA; KAPPA-B; OZONE;
Keywords:
macrophages; inflammatory mediators toxicity;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
58
Recensione:
Indirizzi per estratti:
Indirizzo: Laskin, DL Rutgers State Univ, Environm & Occupat Hlth Sci Inst, 160 Frelinghuysen Rd, Piscataway, NJ 08854 USA Rutgers State Univ 160 Frelinghuysen Rd Piscataway NJ USA 08854
Citazione:
D.L. Laskin e J.D. Laskin, "Role of macrophages and inflammatory mediators in chemically induced toxicity", TOXICOLOGY, 160(1-3), 2001, pp. 111-118

Abstract

Macrophages are critical cellular effecters of nonspecific host defense. They are also potent secretory cells releasing an array of mediators including proinflammatory and cytotoxic cytokines and growth factors, bioactive lipids, hydrolytic enzymes and reactive oxygen and nitrogen intermediates, each of which has been implicated in tissue injury. The research in our laboratories has focused on analyzing the role of macrophages in chemically induced injury in the lung and the liver. In both these tissues, a localized accumulation of macrophages is observed following toxicant exposure. This is directly correlated with the generation of cytotoxic inflammatory mediatorsat these sites. Moreover, when macrophage functioning is blocked, pulmonary and hepatic injury induced by toxicants such as ozone or acetaminophen isprevented. These findings provide direct support for our hypothesis that macrophages contribute to tissue injury. Approaches using pharmacologic inhibitors and transgenic animals are currently being used to evaluate the specific macrophage-derived products involved in the pathogenic process. Our results suggest that the extent to which a particular mediator contributes toinjury depends on the nature of the toxicant, the target tissue, and quantities of the mediator produced. (C) 2001 Elsevier Science Ireland Ltd. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 28/03/20 alle ore 23:43:10