Glutathione reductase activity deficiency in homozygous Gr1a1Neu mice does not cause haemolytic anaemia.
A glutathione reductase (GR) mutant with approximately 50% residual enzyme activity in blood compared with wild-type was detected amongst offspring of isopropyl methanesulphonate-treated male mice. Homozygous mutants with only 2% residual enzyme activity were recovered in progeny of inter se matings of heterozygotes. Results of linkage studies indicate a mutation at the Gr1 structural locus on chromosome 8. The loss of GR activity was evident both in blood and in other tissue extracts. Erythrocyte and organo-somatic indices did not show differences between wild-types and homozygous mutants, indicating no association between the GR deficiency and haemolytic anaemia in this potential animal model.
Pretsch
W
W
GSF-National Research Center for Environment and Health, Institute of Mammalian Genetics, Neuherberg, Germany. pretsch@gsf.de
D000743:Anemia, Hemolytic / Q000201:enzymology / Q000235:genetics; D000818:Animals; D002874:Chromosome Mapping; D005260:Female; D005980:Glutathione Reductase / Q000097:blood / Q000172:deficiency* / Q000235:genetics*; D006720:Homozygote; D008297:Male; D051379:Mice; D008809:Mice, Inbred C3H; D008810:Mice, Inbred C57BL; D008817:Mice, Mutant Strains; D009154:Mutation; D014018:Tissue Distribution
D005980:Glutathione Reductase