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IN VITRO STUDIES OF CEREBRAL CORTICAL RNA AND NUCLEOTIDE METABOLISM IN HYPOTHYROIDISM 1
Author(s) -
Geel S. E.,
Gonzales L. K.
Publication year - 1975
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1975.tb04331.x
Subject(s) - rna , uridine , in vitro , adenosine , ribosomal rna , nucleotide , metabolism , incubation , nucleoside , endocrinology , hormone , medicine , biology , thyroid , biochemistry , chemistry , gene
—Thyroid hormone deficiency induced during the neonatal period in the rat, resulted in an enhanced incorporation of [2‐ 14 C]uridine and [8‐ 14 C]adenosine in vitro into cerebral cortical RNA at 25 days of age. An examination of the acid‐soluble pool constituents separated by polyethyleneiminecellulose TLC, revealed that all phosphorylated derivatives were more highly labelled compared to controls. These differences were not apparent at a lower incubation temperature (4°C). When the average specific activity of precursor pool ATP labelled from adenosine was utilized for the calculation of the rate of RNA synthesis, no change was observed in hypothyroidism. The results are compatible with a maturational‐dependent increase in nucleoside transport and rate of phosphorylation in hypothyroidism which is reflected in the stimulated incorporation into cerebral RNA. The apparent normal rate of RNA synthesis coupled with a diminished cellular RNA concentration in thyroid hormone deficiency, suggests an increased RNA turnover. Experiments with actinomycin D revealed no apparent difference in the rate of decay of rapidly‐labelled (nuclear) RNA. The possibility is discussed that the processing of nuclear RNA, the formation of stable ribosomal complexes and events at the translational level are subject to modification in developing hypothyroid rats.