Affiliation:
1. Department of Child Health, Leicester, U.K.
2. Department of Biochemistry, University of Leicester, Leicester, U.K.
Abstract
1. It has been suggested that low levels of serum caeruloplasmin in Wilson's disease result from the failure to switch from a fetal to an adult mode of caeruloplasmin gene expression. To investigate postnatal expression of the caeruloplasmin gene, steady-state levels of caeruloplasmin messenger RNA in adult and neonatal rat liver were measured.
2. Copper parameters observed in neonatal rats were similar to those seen in Wilson's disease: hepatic copper concentration was significantly elevated (neonatal 164 ± 35 μg/g, adults 50 ± 8 μg/g, P < .001) and serum copper and caeruloplasmin levels were low (neonatal 0.5 ± 0.1 μg/ml, adults 1.3 ± 0.2 μg/ml, P < .001; neonatal 0.20 ± 0.04 arbitrary units, adults 0.69 ± 0.16 arbitrary units, P < .001), respectively.
3. Caeruloplasmin messenger RNA levels were analysed by Northern and dot blotting using a 12P-labelled caeruloplasmin complementary DNA probe. A caeruloplasmin messenger RNA of approximately 4.4 kilobases was detected in both adult and neonatal rat liver, with no significant difference observed in steady-state levels.
4. A step subsequent to caeruloplasmin gene transcription must therefore be impaired in neonatal rats.
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8 articles.
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