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427 The effect of orphenadrine disipal on cell membrane permeability
Abstracts 426 Studies on the Mechanism of Action of TSH in Thyroid Iodide Transport. D. WI. WOODBC’RY, R. KARLER and G. HENINCER (U.S.A.). Stud& in normal, TSH-treated, and hypophysrctomized rats indicate that the thyroid follicular fluid contains more Na- and HCO :I than extracellular fluid whereas follicular cells contain normal concentration of K+. Hypophysectomy, by incrrasing follicular fluid volume and decreasing cell volume, markedly increases .Sa+ and C1 and markedly decreases water and K- concentrations in the thyroid. TSH, by decreacing follicular fluid wlume and increasing crll \~olume, producrs opposite rffccts. HCO :j appears to conccntratc in follicular fluid: hypophysectomy increases HCO n concentration, and decreases iodide concentrating ability; TSH and acetazolamide decrcasc HCO 3 concentration and increase iodide concentrating ability. Thus, HCO :1concrntration apprars to bc inversclp proportional to iodide concentration. Since HCO-, concentration is intimately related to carbonic anhydrase (CA.) activity in other tissurs, C..\. activity of the thyroid \vas measured in diffcrcnt functional states. C.A. activity in follicular cells was clrcrcawd bv TSH and acetazolamide, by prop>-lthiouracil in ‘intact but not hypophysrctomized rats. and by chronic iodide deficiency; all thcsc procrdures increase thyroid iodide uptake. These data suggest that HCO :! normally competes Ivith iodidr for the cellular carrier system which actively transports anions into follicular fluid. HCO :I originates from mrtabolically produced CO, and its concentration is regulated by C.A. TSH and acetazolamide inhibit CA., thereby decreasing HCO, concmtration. Therefore, less HCO-, is available to compete with iodide for the transport system: hence, iodide uptake is increased. Hypophyaectomy produces cffccts opposite to those of TSH and acetazolamide.
427 The Effect of Orphenadrine fDisipa1) on Cell Membrane Permeability. hl. J. E. ERN~ING, \V. F. KMOE, W. T. N.wr.\, H. K. OOSTERHUIS, P. 1\. ROWEMA and C. DE LVAART (Holland). The inhibition by orphenadrine of the oxidative metabolism of brain tissue, metabolizing in vitro, depends on the concentration of the inhibitor. The amino acid lcvcl in the incubation fluid was found to rise more or less parallel with the inhibition. This influence on amino acid metabolism may, among other things, be based on a change in the cell membrane permeability as a result of interference with the energy supply. Shifts in Na and K concentrations point in this direction. We investigated whether these phenomena are connected with ATP formation and whether the permeability for certain dye-stuffs changes accordingly.
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428 Decarboxylation of o-Tyrosine and 5-Hydroxytryptophan by Tissues of Rats Treated with Cortisone and Thyroxine. V. E. DAVIS, C. H.ZNLY and J. I\W.\PARA (U.S..%). hlost tissues of the rat can decarboxylate I.-OThe levels tyrosine and L+hydroxytryptophan. of these activities are somewhat dependent on the concentration of pyridoxal phosphate. Experiments wcrc performed to test the role of cortisone and thyroxine on the decarboxylation of o-tyrosinc and 5.hydroxytryptophan by various organs of the rat. hIale rats (250-3.50 g) werr trrated with cortisone (30 mg/kg) for 10 days. Another group was treated with thyroxine (2.5 mg/ kg) for 16 days. Other groups wrre (a) shamoprratcd, (b‘l adrcnalrctomized, (c) exposed to 4-C, and (d) treated with desoxycorticosterone acetate (10 mg/kg) for 10 days. The rate of decarboxylation of these two substrateq increased up to 60 per cent in the livers of rats treated with cortisone; howevrr, no change of decarboxylase activity was obscrvcd in the kidneys A decrrase of 70 per cent in the activity or brains. \vith o-tyrosine as substrate was noted in the livers of rats treated with thyroxirw. .I decrease in this activity was also observed in the brains of the animals from this group. Livers of adrenalectomized animals given de-ionized watrr showrd a decrease in the rate of dccarboxylation of thcsc Desoxycorticosteronc acetate was withsubstrates. out effect. The action of cortisone on thr decarboxylation of o-tyrosinc and 5hydroxytrytophan seems to be related to changrs in the apoenzyme. The action of thyroxine is now under study.
429 Inhibitory Action of Steroids on Anterior Pituitary Functions. G. GAVAZZI, G. GIULI WI, G. ~IANCILI and I.. MARTINI (Italy). The action of steroids on the release of ACTH and gonadotrophic hormones has been studied in rats. The following procedures were employrd: (a) block of adrenal ascorbic acid depletion in the remaining adrenal 14 hr after unilateral adrenalectomy; (b) drop of blood corticosterone levels as measured by the method of Silber”’ as modified by C;uillemin”’ : (cl block of urinary gonadotrophins output in ovariectomized rats’s’; and (d) decrease of blood LH titres in ovariectomized animals; LH was assayed by the ovarian ascorbic acid method in recipient heavily luteinized rats.‘a’ In the study of ACTH block, the potency of the adrenocortical steroids was as follows: cortisone < hydrocortisone : triamcinolone < prednisone < medrol < Sa-fluorohydrocortisone < prednisolone < A’ Ga-chlorohydrocortisone < oxylone < dexamethasone. Steroids with little or no adrenocortical activity were also found active as ACTH blockers. Total gonadotrophins and LH release inhibition was
427 The Effect of Orphenadrine fDisipa1) on Cell Membrane Permeability. hl. J. E. ERN~ING, \V. F. KMOE, W. T. N.wr.\, H. K. OOSTERHUIS, P. 1\. ROWEMA and C. DE LVAART (Holland). The inhibition by orphenadrine of the oxidative metabolism of brain tissue, metabolizing in vitro, depends on the concentration of the inhibitor. The amino acid lcvcl in the incubation fluid was found to rise more or less parallel with the inhibition. This influence on amino acid metabolism may, among other things, be based on a change in the cell membrane permeability as a result of interference with the energy supply. Shifts in Na and K concentrations point in this direction. We investigated whether these phenomena are connected with ATP formation and whether the permeability for certain dye-stuffs changes accordingly.
of Papers
127
428 Decarboxylation of o-Tyrosine and 5-Hydroxytryptophan by Tissues of Rats Treated with Cortisone and Thyroxine. V. E. DAVIS, C. H.ZNLY and J. I\W.\PARA (U.S..%). hlost tissues of the rat can decarboxylate I.-OThe levels tyrosine and L+hydroxytryptophan. of these activities are somewhat dependent on the concentration of pyridoxal phosphate. Experiments wcrc performed to test the role of cortisone and thyroxine on the decarboxylation of o-tyrosinc and 5.hydroxytryptophan by various organs of the rat. hIale rats (250-3.50 g) werr trrated with cortisone (30 mg/kg) for 10 days. Another group was treated with thyroxine (2.5 mg/ kg) for 16 days. Other groups wrre (a) shamoprratcd, (b‘l adrcnalrctomized, (c) exposed to 4-C, and (d) treated with desoxycorticosterone acetate (10 mg/kg) for 10 days. The rate of decarboxylation of these two substrateq increased up to 60 per cent in the livers of rats treated with cortisone; howevrr, no change of decarboxylase activity was obscrvcd in the kidneys A decrrase of 70 per cent in the activity or brains. \vith o-tyrosine as substrate was noted in the livers of rats treated with thyroxirw. .I decrease in this activity was also observed in the brains of the animals from this group. Livers of adrenalectomized animals given de-ionized watrr showrd a decrease in the rate of dccarboxylation of thcsc Desoxycorticosteronc acetate was withsubstrates. out effect. The action of cortisone on thr decarboxylation of o-tyrosinc and 5hydroxytrytophan seems to be related to changrs in the apoenzyme. The action of thyroxine is now under study.
429 Inhibitory Action of Steroids on Anterior Pituitary Functions. G. GAVAZZI, G. GIULI WI, G. ~IANCILI and I.. MARTINI (Italy). The action of steroids on the release of ACTH and gonadotrophic hormones has been studied in rats. The following procedures were employrd: (a) block of adrenal ascorbic acid depletion in the remaining adrenal 14 hr after unilateral adrenalectomy; (b) drop of blood corticosterone levels as measured by the method of Silber”’ as modified by C;uillemin”’ : (cl block of urinary gonadotrophins output in ovariectomized rats’s’; and (d) decrease of blood LH titres in ovariectomized animals; LH was assayed by the ovarian ascorbic acid method in recipient heavily luteinized rats.‘a’ In the study of ACTH block, the potency of the adrenocortical steroids was as follows: cortisone < hydrocortisone : triamcinolone < prednisone < medrol < Sa-fluorohydrocortisone < prednisolone < A’ Ga-chlorohydrocortisone < oxylone < dexamethasone. Steroids with little or no adrenocortical activity were also found active as ACTH blockers. Total gonadotrophins and LH release inhibition was