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Scobie and Claire Mackinnon Trace Element Laboratory, Murdoch Institute, Royal Children's Hospital, Parkville, Melbourne, Australia, 3052
Normal or mutant pups that nurse dams homozygous for the lethal milk (lm) mutation die as a result of zinc deficiency. Previous determinations of the zinc concentration of the mutant milk have been conflicting. This work demonstrates that the amount of 65Zn recovered in the organs of pups following an intraperitoneal injection of 65Zn to lactating dams was reduced 50–60% in the stomach, 25–30% in the gut and 50–75% in the blood and carcass, for both normal and mutant pups nursing mutant dams, relative to pups nursing normal dams. For pups nursing mutant dams, the zinc concentration of the stomach and contents was determined by atomic absorption spectrometry and found to be 144 nmol/g wet wt (for mutant pups) and 147 nmol/g wet wt (for normal pups). Pups nursing normal dams had stomach zinc concentrations of 322 nmol/g wet wt (mutant pups) and 312 nmol/g wet wt (normal pups). Administration of an oral dose of 65Zn (27 kBq) to normal and mutant adult mice showed that after 24 h there was no significant difference in the distribution of 65Zn in the liver, gut, lung, spleen, kidney, brain, skin, blood, pancreas or heart or in the carcass. We conclude that the major effect of the lethal milk mutation is the production of Zn-deficient milk.
KEY WORDS: • zinc • lethal milk • mice
1 Supported in part by a grant from the National Health and Medical Research Council of Australia and the Scobie and Claire MacKinnon Trust. MLA was supported by a University of Melbourne Postgraduate Research Scholarship.
2 To whom correspondence should be addressed.
Manuscript received 11 October 1991. Revision accepted 9 January 1992.
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