Mechanisms of regulation of ferritin synthesis in rat liver during experimental inflammation.
Liver slices of turpentine-treated rats were incubated in vitro and used as a model to study synthesis and secretion of proteins during the acute-phase response. The synthesis and secretion of typical acute-phase proteins increased after treatment. Similarly, ferritin increased at 24-48 hr after treatment. Serum ferritin showed a slight and transient increase at 6 hr; however, no ferritin was detectable in liver slices medium, indicating no or negligible secretion by this tissue. Northern blot analysis of RNA extracted from total liver homogenate and from free and membrane-bound polyribosomes revealed that turpentine treatment stimulates ferritin synthesis at the translational level, possibly increasing the amount of ferritin mRNA on membrane-bound polysomes.
D000209:Acute-Phase Proteins / Q000096:biosynthesis; D000818:Animals; D056486:Chemical and Drug Induced Liver Injury / Q000378:metabolism*; D005290:Ferric Compounds / Q000494:pharmacology; D005293:Ferritins / Q000096:biosynthesis*; D005786:Gene Expression Regulation; D007249:Inflammation; D007501:Iron / Q000378:metabolism; D008099:Liver / Q000378:metabolism*; D008297:Male; D000644:Quaternary Ammonium Compounds / Q000494:pharmacology; D012333:RNA, Messenger / Q000096:biosynthesis; D051381:Rats; D011919:Rats, Inbred Strains; D014425:Turpentine / Q000633:toxicity
D000209:Acute-Phase Proteins; D005290:Ferric Compounds; D000644:Quaternary Ammonium Compounds; D012333:RNA, Messenger; D005293:Ferritins; D007501:Iron; C013531:ferric ammonium citrate; D014425:Turpentine