Alterations in serum and tissue iron profiles associated with mutations in the fitness1(4226SB) locus of mice

A. E. Schultze, Robert H Poppenga, D. K. Johnson

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

We investigated alterations in serum and tissue iron profiles that were associated with an N-ethyl-N-nitrosourea-induced mutation in the fitness 1 locus in chromosome 7 in mice. Mice hemizygous for the fitness 1 mutation [c fitness1(4226SB)/Df(c Mod2 sh1)(26DVT)] had a microcytic, hypochromic anaemia which was associated with a lower concentration of iron in the serum compared to age-matched, control mice [c(ch)+/c(ch)+]. The hemizygous mutants had a greater total iron binding capacity and an increased unsaturated iron binding capacity compared to controls. The percentage transferrin saturation was significantly decreased in the hemizygous mutant mice compared to control mice. The concentration of iron within several body organs was determined and hemizygous mutant mice had a greater concentration of iron in the liver compared to controls. In contrast, the mutants had a lower concentration of iron within the spleen, kidneys and heart compared to control mice. Microscopic analysis of bone marrow smears indicated less iron in the smears from the hemizygous mutants. From these data, it was concluded that the fitness1(4226SB) mutation in mice causes alterations in the serum iron profile that resemble iron deficiency. The alterations in tissue iron concentrations indicate an abnormal distribution or mobilisation of iron between organ systems. The exact mechanism(s) by which the fitness1(4226SB) mutation mediates these abnormalities in iron distribution remains to be determined.

Original languageEnglish (US)
Pages (from-to)72-76
Number of pages5
JournalComparative Haematology International
Volume8
Issue number2
StatePublished - 1998
Externally publishedYes

Fingerprint

Iron
Mutation
Serum
Ethylnitrosourea
Chromosomes, Human, Pair 7
Transferrin
Spleen
Bone Marrow
Kidney
Liver

Keywords

  • fitness1 locus
  • Iron deficiency
  • Microcytic hypochromic anaemia
  • Serum and tissue iron concentrations

ASJC Scopus subject areas

  • Hematology

Cite this

Alterations in serum and tissue iron profiles associated with mutations in the fitness1(4226SB) locus of mice. / Schultze, A. E.; Poppenga, Robert H; Johnson, D. K.

In: Comparative Haematology International, Vol. 8, No. 2, 1998, p. 72-76.

Research output: Contribution to journalArticle

@article{0df4147f5e8245848a7f174fd514cf05,
title = "Alterations in serum and tissue iron profiles associated with mutations in the fitness1(4226SB) locus of mice",
abstract = "We investigated alterations in serum and tissue iron profiles that were associated with an N-ethyl-N-nitrosourea-induced mutation in the fitness 1 locus in chromosome 7 in mice. Mice hemizygous for the fitness 1 mutation [c fitness1(4226SB)/Df(c Mod2 sh1)(26DVT)] had a microcytic, hypochromic anaemia which was associated with a lower concentration of iron in the serum compared to age-matched, control mice [c(ch)+/c(ch)+]. The hemizygous mutants had a greater total iron binding capacity and an increased unsaturated iron binding capacity compared to controls. The percentage transferrin saturation was significantly decreased in the hemizygous mutant mice compared to control mice. The concentration of iron within several body organs was determined and hemizygous mutant mice had a greater concentration of iron in the liver compared to controls. In contrast, the mutants had a lower concentration of iron within the spleen, kidneys and heart compared to control mice. Microscopic analysis of bone marrow smears indicated less iron in the smears from the hemizygous mutants. From these data, it was concluded that the fitness1(4226SB) mutation in mice causes alterations in the serum iron profile that resemble iron deficiency. The alterations in tissue iron concentrations indicate an abnormal distribution or mobilisation of iron between organ systems. The exact mechanism(s) by which the fitness1(4226SB) mutation mediates these abnormalities in iron distribution remains to be determined.",
keywords = "fitness1 locus, Iron deficiency, Microcytic hypochromic anaemia, Serum and tissue iron concentrations",
author = "Schultze, {A. E.} and Poppenga, {Robert H} and Johnson, {D. K.}",
year = "1998",
language = "English (US)",
volume = "8",
pages = "72--76",
journal = "Comparative Clinical Pathology",
issn = "1618-5641",
publisher = "Springer London",
number = "2",

}

TY - JOUR

T1 - Alterations in serum and tissue iron profiles associated with mutations in the fitness1(4226SB) locus of mice

AU - Schultze, A. E.

AU - Poppenga, Robert H

AU - Johnson, D. K.

PY - 1998

Y1 - 1998

N2 - We investigated alterations in serum and tissue iron profiles that were associated with an N-ethyl-N-nitrosourea-induced mutation in the fitness 1 locus in chromosome 7 in mice. Mice hemizygous for the fitness 1 mutation [c fitness1(4226SB)/Df(c Mod2 sh1)(26DVT)] had a microcytic, hypochromic anaemia which was associated with a lower concentration of iron in the serum compared to age-matched, control mice [c(ch)+/c(ch)+]. The hemizygous mutants had a greater total iron binding capacity and an increased unsaturated iron binding capacity compared to controls. The percentage transferrin saturation was significantly decreased in the hemizygous mutant mice compared to control mice. The concentration of iron within several body organs was determined and hemizygous mutant mice had a greater concentration of iron in the liver compared to controls. In contrast, the mutants had a lower concentration of iron within the spleen, kidneys and heart compared to control mice. Microscopic analysis of bone marrow smears indicated less iron in the smears from the hemizygous mutants. From these data, it was concluded that the fitness1(4226SB) mutation in mice causes alterations in the serum iron profile that resemble iron deficiency. The alterations in tissue iron concentrations indicate an abnormal distribution or mobilisation of iron between organ systems. The exact mechanism(s) by which the fitness1(4226SB) mutation mediates these abnormalities in iron distribution remains to be determined.

AB - We investigated alterations in serum and tissue iron profiles that were associated with an N-ethyl-N-nitrosourea-induced mutation in the fitness 1 locus in chromosome 7 in mice. Mice hemizygous for the fitness 1 mutation [c fitness1(4226SB)/Df(c Mod2 sh1)(26DVT)] had a microcytic, hypochromic anaemia which was associated with a lower concentration of iron in the serum compared to age-matched, control mice [c(ch)+/c(ch)+]. The hemizygous mutants had a greater total iron binding capacity and an increased unsaturated iron binding capacity compared to controls. The percentage transferrin saturation was significantly decreased in the hemizygous mutant mice compared to control mice. The concentration of iron within several body organs was determined and hemizygous mutant mice had a greater concentration of iron in the liver compared to controls. In contrast, the mutants had a lower concentration of iron within the spleen, kidneys and heart compared to control mice. Microscopic analysis of bone marrow smears indicated less iron in the smears from the hemizygous mutants. From these data, it was concluded that the fitness1(4226SB) mutation in mice causes alterations in the serum iron profile that resemble iron deficiency. The alterations in tissue iron concentrations indicate an abnormal distribution or mobilisation of iron between organ systems. The exact mechanism(s) by which the fitness1(4226SB) mutation mediates these abnormalities in iron distribution remains to be determined.

KW - fitness1 locus

KW - Iron deficiency

KW - Microcytic hypochromic anaemia

KW - Serum and tissue iron concentrations

UR - http://www.scopus.com/inward/record.url?scp=0031903747&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0031903747&partnerID=8YFLogxK

M3 - Article

VL - 8

SP - 72

EP - 76

JO - Comparative Clinical Pathology

JF - Comparative Clinical Pathology

SN - 1618-5641

IS - 2

ER -