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Glutathione reductase activity deficiency in homozygous Gr1a1Neu mice does not cause haemolytic anaemia

Published online by Cambridge University Press:  01 February 1999

WALTER PRETSCH
WALTER PRETSCH
Affiliation:
GSF–National Research Center for Environment and Health, Institute of Mammalian Genetics, Ingolstädter Landstrasse 1, D-85764 Neuherberg, Germany
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Abstract

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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.

Type
Research Article
Information
Genetics Research , Volume 73 , Issue 1 , February 1999 , pp. 1 - 5
Copyright
© 1999 Cambridge University Press