Effects of hypophysectomy and triiodothyronine on de novo biosynthesis, catalytic activity, and estrogen induction of rat liver histidase.

E.G Armstrong,M Feigelson

doi:10.1016/s0021-9258(20)79685-7

Abstract

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.

Highlights

Monal control; estrogen, glucocorticoid, and glucagon, acting extra-adrenally, and growth hormone each decrease via CAMP,induce this enzyme
The presence of the pituitary [12,13,14,15,16,17] and administration of thyroid hormone [17,18,19,20,21,22,23,24,25] are both known to enhance the activities and syntheses of many hepatic enzymes and to promote generalized protein synthetic activity in liver.The present studies explore the mechanisms by which hypophymone may be primaryin the hypophyseal suppression sectomy elevates and 3,5,3’-triiodothyronine (TRd)iminishes of histidase
Catalytic Activity and Synthesis inHypophysectomized Rats-In order to ascertain whether hypophyseal suppression of hepatic histidase activity and biosynthesis couldbe the result of thyroid hormone action, histidase catalytic activities and ratesof synthesis, relative to totalsoluble protein synthesis, were determined in livers of hypophysectomized adult males which had received eight daily injections of increasing doses of T3 (Fig. 3A)

Summary

Glenn Armstrongf andMuriel Feigelsong

From the Departmentsof Biochemistry a n d of Obstetrics and Gynecology, Columbia University College of Physicians and Surgeons, Roosevelt Hospital, New York, New York 10019. These responses of Treatment of hypophysectomized rats with physiological levels of triiodothyronine (T3)diminished histidase synthetic rates and catalyticactivitiesto normal levels, despite concomitant elevation in total soluble protein synthesis. The presence of the pituitary [12,13,14,15,16,17] and administration of thyroid hormone [17,18,19,20,21,22,23,24,25] are both known to enhance the activities and syntheses of many hepatic enzymes and to promote generalized protein synthetic activity in liver.The present studies explore the mechanisms by which hypophymone may be primaryin the hypophyseal suppression sectomy elevates and 3,5,3’-triiodothyronine (TRd)iminishes of histidase. Selective increases in hepatic histidase catalytic activity are observed following hypophysectomy ( 7 ) , indicating that the

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