Effects of hypophysectomy and triiodothyronine on de novo biosynthesis, catalytic activity, and estrogen induction of rat liver histidase
| Autor: | E G Armstrong, M Feigelson |
|---|---|
| Rok vydání: | 1980 |
| Předmět: |
chemistry.chemical_classification
medicine.medical_specialty Triiodothyronine Hypophysectomy medicine.drug_class medicine.medical_treatment Cell Biology Biology Biochemistry Glucagon Prolactin Endocrinology Enzyme chemistry Estrogen Internal medicine medicine Molecular Biology Glucocorticoid medicine.drug Hormone |
| Zdroj: | Journal of Biological Chemistry. 255:7199-7203 |
| ISSN: | 0021-9258 |
| DOI: | 10.1016/s0021-9258(20)79685-7 |
| Popis: | Synthesis of rat liver histidase is under multihormonal control; estrogen, glucocorticoid, and glucagon, via cAMP, induce this enzyme. By means of in vivo [3H]leucine incorporation into immunoprecipitated histidase, relative to that incorporated into total soluble protein, we have now demonstrated that de novo hepatic histidase synthesis, as well as catalytic activity, is selectively increased following hypophysectomy. Treatment of hypophysectomized rats with physiological levels of triiodothyronine (T3) diminished histidase synthetic rates and catalytic activities to normal levels, despite concomitant elevation in total soluble protein synthesis. Thyrotoxic doses of T3 further reduced histidase synthesis to barely measurable rates. Since thyroid hormone is under pituitary regulation, this hormone may be primary in the hypophyseal suppression of histidase. Estrogen does not induce hepatic histidase in the hypophysectomized rat. However, administration of the histidase suppressor, T3, or prolactin, which in itself has no effect on this enzyme, was ineffective in reinstating estrogen inducibility of histidase in the hypophysectomized animal. Thus, some as yet unknown hypophyseal agent is required for estrogenic inducibility of this liver enzyme. |
| Databáze: | OpenAIRE |
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