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T Pribyl

Publications and source records attributed to T Pribyl.

At least 55 records · Page 3Linked to original sources
PubMed1980

Inhibition of rat serum polyphenoloxidase activity by silver ions abolished by administration of copper ions.

The administration of silver nitrate (6.47 mg, i.e. 60 mumol Ag+/rat/day) in food was followed in only two days by a pronounced decrease in polyphenoloxidase activity (ceruloplasmin) in rat serum. The administration of copper in the form of copper sulphate (12.7 mg, i.e. 200 mumol Cu2+/rat/day) raised polyphenoloxidase activity (the ceruloplasmin level), the increase being particularly marked on the first four days. On combining the two factors, the effect of Cu+ predominated throughout the duration of the experiment (32 days).

Animals↗
PubMed1980

Partial inhibition of oestrogen-induced adenohypophyseal growth by silver nitrate.

The administration of silver nitrate to rats in their food (10 mg/rat/day) led to the rapid disappearance of serum polyphenol oxidase activity. After 60 days silver nitrate treatment produced a decrease of adenohypophyseal weight. If given over a period of 40--60 days it also partially inhibited the adenohypophyseal response to oestradiol (a weight decrease and raised thyroxine binding by adenohypophyseal proteins in vitro). The mechanism by which silver nitrate diminishes basal and oestrogen-increased adenohypophyseal weight remains unknown.

Animals↗
PubMed1980

Modulation oestradiol effects by silver nitrate: inhibition of the adenohypophyseal reaction, block of the ceruloplasmin increase and block of hypothalamic ascorbic acid depletion.

Chronic oestradiol treatment (1 mg oestradiol benzoate, as an aqueous microcrystal suspension, i.m. twice a week for 6 weeks) produces in rats increased thyroxine-binding capacity of the adenohypophyseal proteins in vitro, an increase in the ceruloplasmin (polyphenol oxidase) level in blood and a decrease in the hypothalamic ascorbic acid concentration. The simultaneous administration of silver nitrate (10mg/rat/day in food) inhibits all these reactions in oestradiol. Apart from inhibiting blood polyphenol oxidase activity, silver nitrate itself has no effect. The possibility of the interaction of polyphenol oxidase(ceruloplasmin), silver nitrate and hypothalamic ascorbic acid in the dopaminergic modulation of the adenohypophyseal reaction to oestradiol is discussed.

Animals↗
PubMed1979

Effect of dopamine-beta-hydroxylase inhibitor (disulfiram) on the response of adenohypophysis, serum ceruloplasmin and hypothalamic ascorbic acid to estradiol treatment.

The administration of tetraethylthiuramdisulfide (disulfiram, Antabus--inhibitor of dopamine-beta-hydroxylase) resulted in an inhibition of the response of anterior pituitary to estradiol (i. e. increase of weight and of binding capacity of anterior pituitary proteins to thyroxine). At the same time there was no inhibition of an increase of ceruloplasmin (polyphenoloxidase) level after estradiol, while a decrease of ascorbic acid in hypothalamus was fully prevented. It was concluded that disulfiram may inhibit dopamine-beta-hydroxylase activity and thus presumably protect the hypothalamic dopamine which further inhibits the response of anterior pituitary to estradiol either directly or through a dopamine dependent growth inhibiting factor.

Animals↗
PubMed1978

The effect of hexose monophosphate shunt inhibitors on adenohypophyseal and ceruloplasmin reactions to oestrogen.

Oestradiol benzoate, as an aqueous microcrystal suspension, was administered i.m. to rats in doses of 1 mg twice a week; it induced adenohypophyseal hyperplasia and an increase of the thyroxine-binding capacity of the adenohypophyseal proteins in vitro and raised the blood ceruloplasmin level. The simultaneous administration of a hexose monophosphate shunt inhibitor--6-aminonicotinamide (200 microgram/rat/day in food) or oxythiamine (8 mg/rat/day in food)--did not modify the reaction of the adenohypophysis; the hexose monophosphate shunt thus probably does not play a significant role in the adenohypophyseal reaction to oestrogens. By themselves, both inhibitors raised the blood ceruloplasmin level and their effect summated with that of oestradiol. The mechanism of action of the inhibitors is not known, but a nonspecific stress effect leading to an increase in the ceruloplasmin level as an "acute phase protein" is considered to be the most likely.

6-Aminonicotinamide↗
PubMed1978

Dopaminergic control of adenohypophyseal growth after oestrogens: negative results with L-DOPA, RO-4-4602, alpha-methyl-DOPA, apomorphine, haloperidol, pyridoxine and cyproheptadine.

Chronic oestrogen treatment augments adenohypophyseal weight and the thyroxine-binding capacity of adenohypophyseal proteins in rats. Since these reactions are both inhibited by ergocornine and ergoline derivatives (as well as by the thyroid hormones, testosterone, anti-oestrogens and antiandrogens), and are potentiation by perphenazine and the dopaminergic neurone blocker Pimozide, the peroral effectiveness of various other substances presumed to act in the region of the dopaminergic or serotoninergic neurones of the hypothalamus was tested. L-DOPA (10 mg/rat/day) did not modify the adenohypophyseal reaction, either alone or combined with the DOPA-decarboxylate inhibitor Ro-4-4602 (1 mg/rat/day). alpha-Methyl-DOPA (10 mg/rat/day), apomorphine (3 mg/rat/day), haloperidol (0.2 mg/rat/day), pyridoxine (20 mg/rat/day) and cyproheptadine (1 mg/rat/day) were likewise ineffective.

Animals↗
PubMed1978

Increase of ceruloplasmin level in blood of rats after ACTH.

The level of ceruloplasmin in plasma was measured as polyphenol oxidase activity in following groups of rats: 1. controls; 2. adrenalectomized; 3. shamadrenalectomized; 4. formalin arthritis; 5. ACTH treated (25 micrograms ACTH daily for 5 days); 6. adrenalectomized and ACTH treated (as in a previous group). The level of ceruloplasmin was markedly increased after formalin arthritis, after ACTH treatment in controls and in adrenalectomized animals.

Adrenal Glands↗
PubMed1978

Serum polyphenol oxidase activity (ceruloplasmin) in conventional laboratory animals and man.

The optimum pH for ceruloplasmin as polyphenol oxidase (EC 1.10.3.2) activity was determined in human serum (pH 5.4) and the serum of conventional laboratory animals--the rat (pH 5.2), mouse (pH 5.2), hamster (pH 5.3), guinea pig (pH 5.4), multimammate mouse (pH 5.2) and rabbit (pH 5.4). Determined at the optimum pH in 0.1M acetate buffer polyphenol oxidase activity fell in the sequence: rat--man--rabbit--mouse--multimammate mouse--hamster--guinea pig. Ceruloplasmin polyphenol oxidase activity was inhibited by 0.1M phosphate buffer in the mouse, rat and multimammate mouse, but not in the other species. It was inhibited by 0.05M citrate and 0.1M phthalate buffer in all the species tested.

Animals↗
PubMed1977

Effect of interaction of oestrogen, testosterone and thyroid hormones on the serum ceruloplasmin level in rats.

Male rats were given oestradiol benzoate (1 mg as an aquaeous microcrystal suspension i.m. twice a week), testosterone isobutyrate (0.5 mg as an aquaeous microcrystal suspension i.m. once a week) and dried thyroid (Thyreoidin SPOFA, 0.2% in food), alone or variously combined. Oestradiol raised adenohypophyseal weight, the binding capacity of the adenohypophyseal proteins for thyroxine and the serum ceruloplasmin level. Testosterone and Thyreoidin inhibited all three of these reactions, but when they were administered together there was no summation of their inhibitory action. The nature of the relationships between the three given proteosynthetic reactions is discussed.

Animals↗
PubMed1977

Interaction of perphenazine and an ergoline derivative on oestrogen-induced adenohypophyseal growth.

Male and female rats were injected twice a week for three weeks with doses of 1 mg oestradiol benzoate (OE), were given perphenazine (P, 2 mg/rat/day) or the ergoline derivative D-6-methyl-8-ergoline-(I)-yl acetic acid amide (Deprenon SPOFA, D, 200 microng/rat/day) in their food or were treated with various combinations of all three factors. OE-induced adenohypophyseal growth was inhibited by D, but the inhibitory effect of D was completely suppressed by P. D also inhibited the OE-induced increase in the thyroxine-binding capacity of the adenohypophyseal proteins, but this inhibition was not suppressed by the simultaneous administration of P. The administration of OE was followed by elevation of the serum ceruloplasmin level, which was not inhibited by P or D, either alone or combined. Ovarian weight rose markedly after D and the increase was inhibited by the simultaneous administration of either OE or P.

Adrenal Glands↗
PubMed1977

Effect of oestrogen and ascorbic acid on the serum ceruloplasmin level in rats.

The administration of long-acting oestrogen (1 mg twice a week for 3 weeks) is followed, in rats, by an increase in the serum ceruloplasmin concentration to about 150% of the control value. The simultaneous administration of ascorbic acid in a dose of 10, 20 or 50 mg/rat/day in food raises the ceruloplasmin concentration to 180-200% of the control value (no significant difference was observed in the effect of the various doses of ascorbic acid). The increase produced by combining ascorbic acid with the oestrogen amounts to 20-30% of the value recorded in animals treated only with oestrogen. The mechanism by which ascorbic acid potentiates the effect of oestrogens on the ceruloplasmin level is not known.

Animals↗
PubMed1977

Antioestrogenic action of the aldosterone antagonist canrenoate K in the rat (adenohypophysis, ceruloplasmin).

In a dose of 7,k mg/rat/day in food, the aldosterone antagonist canrenoate K inhibited the adenohypophyseal reaction (growth, raised thyroxine-binding capacity of the adenohypophyseal proteins in vitro) and the ceruloplasmin reaction (elevation of the serum ceruloplasmin level) to three weeks' intramuscular administration of long-acting oestradiol benzoate in doses of 1 mg twice a week. The effect was similar to that of the antioestrogen clomiphen in a dose of 1.25 mg/rat/day in food. In combined administration of clomiphen and canrenoate K, no summation of their effect was observed. Neither canrenoate nor clomiphen affected the post-oestradiol drop in body weight, but they both potentiated the oestradiol-induced decrease in testicular weight and canrenoate potentiated the effect of oestradiol on uterine weight. It was therefore concluded that the effect of canrenoate is not of a catatoxic nature, i.e. that it is not determined by increased metabolic degradation of oestradiol.

Animals↗