title: Gene expression of iron-related proteins during iron deficiency caused by scurvy in guinea pigs.
abstract: The regulation of expression of hepatic iron-related proteins was examined during iron deficiency caused by scurvy in guinea pigs. Previous studies showed that some effects of scurvy, such as suppression of collagen gene expression, result from events associated with weight loss. During the initial phase of scurvy when vitamin C is depleted but animals grow normally, serum iron levels decreased to 50% of normal. During the second phase of scurvy when animals lose weight, there was a further decrease in iron levels to 10-15% of normal. Serum transferrin levels increased during scurvy, but this increase was related neither to the rate of weight loss nor to hepatic transferrin mRNA expression, which decreased. Serum ferritin levels of diminished early in scurvy with a preferential loss of the L subunit. In liver, however, both ferritin animals gaining weight. Ferritin gene expression during vitamin C deficiency was correlated with serum ferritin levels in that the level of mRNA for the H subunit remained relatively constant while that of the L subunit decreased early. Transferrin receptor mRNA expression in liver was induced as soon as iron levels decreased early in scurvy, which is similar to results reported for iron-depleted cultured cells. In contrast to results in cell culture, expression of iron regulatory protein 1 mRNA was decreased to approximately 50% of normal early in scurvy with a concomitant decrease in hepatic cytosolic aconitase activity. Our data indicate that iron deficiency occurs early during vitamin C deficiency and leads to changes in expression of iron-related proteins that differ in some aspects from regulation by iron in cell culture. Other events associated with weight loss in late scurvy may play a further role in this regulation.
authors.affiliation: Laboratory of Biochemistry, National Cancer Institute, Bethesda, Maryland 20892-4255, USA.
authors.forename: A
authors.initials: A
authors.lastname: Gosiewska
authors.forename: F
authors.initials: F
authors.lastname: Mahmoodian
authors.forename: B
authors.initials: B
authors.lastname: Peterkofsky
mesh_terms: D000154:Aconitate Hydratase / Q000378:metabolism; D000595:Amino Acid Sequence; D000818:Animals; D001483:Base Sequence; D003600:Cytosol / Q000201:enzymology; D018076:DNA, Complementary / Q000235:genetics; D005293:Ferritins / Q000737:chemistry / Q000235:genetics; D005786:Gene Expression Regulation; D006168:Guinea Pigs; D007501:Iron / Q000097:blood; D000090463:Iron Deficiencies; D035925:Iron-Regulatory Proteins; D008099:Liver / Q000378:metabolism; D008969:Molecular Sequence Data; D015345:Oligonucleotide Probes / Q000235:genetics; D011487:Protein Conformation; D011506:Proteins / Q000235:genetics* / Q000378:metabolism; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D016601:RNA-Binding Proteins / Q000097:blood / Q000235:genetics; D011990:Receptors, Transferrin / Q000235:genetics; D012614:Scurvy / Q000150:complications / Q000235:genetics* / Q000378:metabolism; D014168:Transferrin / Q000235:genetics / Q000378:metabolism; D015431:Weight Loss / Q000502:physiology
chemical_list: D018076:DNA, Complementary; D035925:Iron-Regulatory Proteins; D015345:Oligonucleotide Probes; D011506:Proteins; D012333:RNA, Messenger; D016601:RNA-Binding Proteins; D011990:Receptors, Transferrin; D014168:Transferrin; D005293:Ferritins; D007501:Iron; D000154:Aconitate Hydratase