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A Caenorhabditis elegans Nutritional-status Based Copper Aversion Assay
Published on: July 26, 2017
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Failure to confirm abnormal copper utilization in crinkler (cr) mice
J R Mann1, J Camakaris, J M Gillespie
1Genetics Research Unit, Royal Children's Hospital, Parkville, Victoria, Australia.
Biological Trace Element Research
|November 26, 2013
Summary
Crinkled mice symptoms are not caused by copper deficiency. Studies found normal copper levels and utilization in crinkled mice, indicating other factors are responsible for their condition.
Area of Science:
- Biochemistry
- Genetics
- Cell Biology
Background:
- Crinkled (cr/cr) mice exhibit symptoms attributed to copper deficiency.
- Previous research suggested a link between crinkled mouse phenotype and impaired copper metabolism.
Purpose of the Study:
- To investigate copper utilization in crinkled mice.
- To determine if copper deficiency underlies the crinkled mouse phenotype.
Main Methods:
- Assessed copper concentrations in various tissues and cell types.
- Measured serum ceruloplasmin oxidase activity.
- Analyzed copper binding and elution profiles.
- Evaluated effects of copper supplementation.
- Examined hair sulfhydryl groups and skin histology.
- Assessed lysyl oxidase activity and brain myelin composition.
Main Results:
- Normal copper levels were observed in liver, kidney, brain, fibroblasts, and epithelial cells.
- Serum ceruloplasmin oxidase activity was normal.
- Copper supplementation did not reduce mortality.
- No abnormalities were found in hair, skin, lysyl oxidase activity, or brain myelin.
- Gel-filtration chromatography showed no differences in bound copper elution.
Conclusions:
- The crinkled mouse phenotype is not caused by copper deficiency.
- Copper metabolism and utilization appear normal in crinkled mice.
- The underlying cause of crinkled mouse symptoms requires further investigation beyond copper status.
