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HEPATIC METALLOTHIONEIN INDUCTION IN INFLAMMATION * †
Author(s) -
Sobocinski P. Z.,
Canterbury W. J.
Publication year - 1982
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.1982.tb22149.x
Subject(s) - accreditation , medicine , library science , gerontology , management , medical education , economics , computer science
Numerous chemically distinct phlogistic substances have been shown to induce hepatic metallothionein-Zn (MT) accumulation when administered to rats. These findings suggest that induction of this cysteine-rich metalloprotein occurs through the action of some common mediator(s). Possible mediators include substances such as leukocytic endogenous mediator (LEM) and/or hormones known to influence hepatic protein synthesis. Studies were performed to examine further the mechanism(s) and potential mediators involved in endotoxin-induced MT accumulation. Additionally, the studies were performed to determine the possible involvement of genetic factors, which reportedly influence LEM production, in the induced MT response. Endotoxin (ET) was administered ip to rats and to EP-resistant, C3H/HeJ, and susceptible, C3Heb/FeJ, stains of mice. ET induced hypozincemia, hyperglucagonemia, and increased MT concentrations in rats. ET induced hypozincemia and MT accumulation to the same extent in both strains of mice. The induction of tolerance in rats to Zn depressing activity of ET also prevented hyperglucagonemia and additional accumulation of MT. Results suggest that glucagon, but not LEM, may be a common mediator in MT response during inflammatory stress.