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Hepatic metallothionein induction in inflammation

P Z Sobocinski, W J Canterbury

    Annals of the New York Academy of Sciences
    |January 1, 1982
    PubMed
    Summary

    Endotoxin (ET) triggers hepatic metallothionein-Zn (MT) accumulation in rats, mediated by glucagon, not leukocytic endogenous mediator (LEM). Genetic factors did not influence this MT response in mice.

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    Area of Science:

    • Biochemistry
    • Toxicology
    • Immunology

    Background:

    • Phlogistic substances can induce hepatic metallothionein-Zn (MT) accumulation.
    • This induction is thought to involve common mediators like leukocytic endogenous mediator (LEM) or hormones.
    • Endotoxin (ET) is a potent inducer of inflammatory responses and MT accumulation.

    Purpose of the Study:

    • To investigate the mechanisms and mediators of endotoxin-induced MT accumulation.
    • To determine the role of genetic factors in the MT response to endotoxin.
    • To differentiate the roles of potential mediators, specifically glucagon and LEM.

    Main Methods:

    • Administration of endotoxin (ET) to rats and two strains of mice (C3H/HeJ and C3Heb/FeJ).
    • Measurement of hypozincemia, hyperglucagonemia, and hepatic MT concentrations.
    • Induction of tolerance to ET in rats to assess its effect on mediators and MT accumulation.

    Main Results:

    • ET induced hypozincemia, hyperglucagonemia, and increased MT in rats.
    • Both endotoxin-resistant and susceptible mouse strains showed similar ET-induced hypozincemia and MT accumulation.
    • Tolerance to ET in rats blocked hyperglucagonemia and further MT accumulation.

    Conclusions:

    • Glucagon, not LEM, appears to be a key mediator in the endotoxin-induced MT response during inflammatory stress.
    • Genetic factors influencing LEM production do not seem to play a significant role in ET-induced MT accumulation.
    • These findings elucidate the hormonal pathways involved in the hepatic response to endotoxin.

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