Accession Number:

ADA123105

Title:

Hepatic Metallothionein Induction in Inflammation

Descriptive Note:

Journal article

Corporate Author:

ARMY MEDICAL RESEARCH INST OF INFECTIOUS DISEASES FORT DETRICK MD

Report Date:

1982-01-01

Pagination or Media Count:

15.0

Abstract:

Hypozincemia as a consequence of the movement of endogenous zinc from plasma to liver during inflammatory stress is well known. The redistributed zinc is sequestered in the liver, by a unique pleomorphic metalloprotein, metallothionein. The mechanisms involved in the de novo synthesis of metallothionein has been the subject of extensive studies since it appears to be intimately involved in zinc homeostasis in normal, pathophysiologic, and stress conditions. Since hepatic accumulation of metallothionein occurs during the early phase of inflammatory stresses, such as bacterial infection and endotoxemia, it appears that it can be appropriately classified as an acute phase alteration. The stimulus which triggers hepatic metallothionein synthesis in these diverse conditions remains unknown. Its synthesis and accumulation apparently are not in every instance dependent on the presence of inflammatory stress since hepatic accumulation has been reported during other stresses such as exposure to cold environment and exercise. Identification of a common endogenous mediator for hepatic metallothionein synthesis has not been conclusively demonstrated. In contrast, existence of a common endogenous mediator influencing hepatic synthesis of certain plasma acute-phase proteins appears to be established. The latter mediator has been termed leukocytic endogenous mediator LEM although its exact chemical characterization remains elusive and controversial. Experimental evidence indicating that LEM mediates hepatic synthesis of the intracellular protein, metallothionein, is lacking, although it induces hypozincemia and a cascade of other acute-phase alterations when administered to rats.

Subject Categories:

  • Biochemistry
  • Medicine and Medical Research

Distribution Statement:

APPROVED FOR PUBLIC RELEASE