Increase In Ferritin Synthesis Research Articles

The relationship between iron release, ferritin synthesis and intracellular iron distribution in mouse peritoneal macrophages. Evidence for a reduced level of metabolically available iron in elicited macrophages

The rate of iron release from thioglycollate-elicited mouse peritoneal macrophages pulsed with 59Fe-labelled transferrin-antitransferrin immune complexes was lower than that from resident or Corynebacterium parvum-activated macrophages. Anaerobic conditions increased the rate of iron release by thioglycollate-elicited macrophages but had no effect on resident or C. parvum-activated macrophages. Thioglycollate-elicited macrophages also contained less ferritin and were deficient in their ability to synthesise ferritin. Incubation of these cells in medium containing 100 μM iron caused some increase in ferritin synthesis, but the response to iron was much less pronounced than that by resident or C. parvum-activated macrophages. In the thioglycollate-elicited macrophages, relatively less iron was incorporated into ferritin, and more into other soluble macromolecules and insoluble haemosiderin-like compounds than in the other types of macrophages. It is proposed that thioglycollate-elicited macrophages tend to divert iron to a relatively inert intracellular pool, and that this could account for their reduced ability to release iron. Such a mechanism might help to explain the reduced release of iron by liver and spleen macrophages occurring during inflammation.

Ferritin Synthesis in Inflammation: I. PATHOGENESIS OF IMPAIRED IRON RELEASE

Plasma iron turnover (PIT) and ferritin synthesis in the liver and spleen were studied in rats within the first 24 h of inflammation produced by turpentine injection. Comparison of the sequential changes in PIT and ferritin synthesis showed that alterations in ferritin synthesis preceded the changes in plasma iron exchange throughout the study. Thus, after 4 h inflammation ferritin synthesis was twice normal whereas plasma iron and PIT were still unchanged. Conversely, maximal reduction in plasma iron occurred after 12 h inflammation, at a time when ferritin synthesis had already declined to normal rates. These correlations seem to indicate that, in analogy with other acute phase reacting proteins, increased ferritin synthesis is a primary nonspecific response which is part of a general pattern of the systemic effects of inflammation. This increase in ferritin synthesis is assumed to be responsible for the diversion of labile iron into ferritin stores, and its reduced availability for release from tissues.