Related Experiment Videos
Hepatic metallothionein induction in inflammation
Annals of the New York Academy of Sciences
|January 1, 1982
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.
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.