Metabolism of 25-hydroxyvitamin D in copper-laden rat: A model of Wilson's disease
- Harvard Medical School, Boston (USA) Yale Univ. School of Medicine, New Haven, CT (USA)
Wilson's disease results in excess tissue accumulation of copper and is often complicated by skeletal and mineral abnormalities. The authors investigated vitamin D metabolism in rats fed a copper-laden diet rendering hepatic copper content comparable with that found in Wilson's disease. Injection of 25-hydroxyvitamin D{sub 3} (25(OH)D{sub 3}) resulted in reduced 1,25--dihydroxyvitamin D (1,25(OH){sub 2}D) levels in copper-intoxicated rats. In vitro 25(OH)D-1{alpha}-hydroxylase activity was impaired in renal mitochondria from copper-intoxicated animals. Activity was also inhibited in mitochondrial from controls when copper was added to incubation media. Impaired conversion of 25(OH)D to 1,25(OH){sub 2}D occurs in copper intoxication and suggests that altered vitamin D metabolism is a potential factor in the development of bone and mineral abnormalities in Wilson's disease.
- OSTI ID:
- 6948881
- Journal Information:
- American Journal of Physiology; (USA), Vol. 254:2; ISSN 0002-9513
- Country of Publication:
- United States
- Language:
- English
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COPPER COMPOUNDS
BIOLOGICAL EFFECTS
HYDROXYLASES
ENZYME ACTIVITY
SKELETAL DISEASES
PATHOGENESIS
VITAMIN D
METABOLISM
CHOLECALCIFEROL
KIDNEYS
MITOCHONDRIA
PARATHORMONE
RADIOCHROMATOGRAPHY
RATS
TRITIUM COMPOUNDS
ANIMALS
BODY
CELL CONSTITUENTS
CHROMATOGRAPHY
DISEASES
ENZYMES
HORMONES
HYDROGEN COMPOUNDS
MAMMALS
ORGANOIDS
ORGANS
OXIDOREDUCTASES
PEPTIDE HORMONES
RODENTS
SEPARATION PROCESSES
TRANSITION ELEMENT COMPOUNDS
VERTEBRATES
VITAMINS
550201* - Biochemistry- Tracer Techniques