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

A. M. Konijn, C. Hershko*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

238 Scopus citations

Abstract

Summary. 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.

Original languageEnglish
Pages (from-to)7-16
Number of pages10
JournalBritish Journal of Haematology
Volume37
Issue number1
DOIs
StatePublished - Sep 1977

Fingerprint

Dive into the research topics of 'Ferritin Synthesis in Inflammation: I. PATHOGENESIS OF IMPAIRED IRON RELEASE'. Together they form a unique fingerprint.

Cite this