The Jackson toxic milk mouse as a model for copper loading

The Jackson toxic milk mouse as a model for copper loading Short Communications Incorporating Mouse Genome Mammalian Genome 12, 793–795 (2001). © Springer-Verlag New York Inc. 2001 DOI: 10.1007/s00335-001-3021-y Veronica Coronado, Manoj Nanji, Diane W. Cox Department of Medical Genetics, University of Alberta, Edmonton, AB, Canada T6G 2H7 Received: 27 February 2001 / Accepted: 25 May 2001 Copper is an essential trace element required for the normal bio- born of homozygous tx dams are severely copper deficient and logical function of several prokaryotic and eukaryotic enzymes. display growth retardation, hypopigmentation, and death by 2 However, when present in excess, copper becomes toxic, cata- weeks of age (Rauch 1983). lyzing the production of highly reactive oxygen species, including In 1987, a new autosomal recessive mutation (tx ) arose in the the conversion of hydrogen peroxide to hydroxyl radical (Halliwell C3H/HeJ animal resources colony at The Jackson Laboratory, Bar and Gutteridge 1984). Excessive production of free radicals can Harbor, Maine (Sweet and Davisson 1989). As with the tx/tx mu- result in tissue damage due to oxidative stress. Recently, free radi- tant, adult homozygous tx mice develop cirrhosis, and infant mice cal-induced oxidative stress has been implicated in a variety of are pale colored, copper deficient, and display early mortality neurological disorders, including Mammalian Genome Springer Journals

The Jackson toxic milk mouse as a model for copper loading

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Copyright © 2001 by Springer-Verlag New York Inc.
Life Sciences; Cell Biology; Anatomy; Zoology
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