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The pathology and trace element status of the toxic milk mutant mouse
1School of Veterinary Studies, Murdoch University, Australia.
Abstract:
The toxic milk (tx) mouse is a mutant in which copper metabolism is abnormal. Homozygous tx adults do not show overt signs of disease, but litters born to such parents are deficient in copper and die at about 2 weeks of age unless copper is provided. The results reported here clearly indicate that adults accumulate copper in the liver, kidney, spleen, brain, muscle, serum and red blood cells. The concentration of zinc is also elevated in liver, brain and muscle. In adult animals there is damage to hepatocytes with marked changes to the nuclei. Haemolysis occurs with subsequent deposition of haemosiderin in the kidney. This mutant provides a useful model for studies of the pathogenesis and treatment of copper toxicity in animals and man.
Insights
The toxic milk (tx) mouse mutant exhibits abnormal copper metabolism, leading to copper accumulation and toxicity in adults. Offspring from these mice show copper deficiency and mortality without supplementation.
Area of Science:
- Biochemistry
- Genetics
- Toxicology
Background:
- The toxic milk (tx) mouse is a genetic mutant with impaired copper metabolism.
- Homozygous tx adults are asymptomatic but produce copper-deficient offspring.
- Copper deficiency in offspring leads to mortality around two weeks of age without intervention.
Purpose of the Study:
- To investigate the physiological and pathological consequences of abnormal copper metabolism in the toxic milk (tx) mouse model.
- To characterize the distribution and effects of copper and zinc accumulation in tx mice.
Main Methods:
- Analysis of copper and zinc concentrations in various tissues and blood components of homozygous tx mice.
- Histopathological examination of liver and kidney tissues to assess cellular damage.
- Observation of offspring viability and response to copper supplementation.
Main Results:
- Adult tx mice accumulate significant levels of copper in the liver, kidney, spleen, brain, muscle, serum, and red blood cells.
- Elevated zinc concentrations were observed in the liver, brain, and muscle of tx mice.
- Hepatocyte damage, nuclear changes, and kidney haemosiderin deposition due to hemolysis were evident in adult tx mice.
Conclusions:
- The toxic milk (tx) mouse serves as a valuable model for studying copper toxicity pathogenesis.
- This mutant offers insights into copper and zinc dysregulation and associated organ damage.
- Findings support the utility of the tx mouse for research into copper toxicity treatments in both animals and humans.