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V Schreiber

Publications and source records attributed to V Schreiber.

33 records · Page 2Linked to original sources
PubMed1977

Chromosomal changes in rat pituitary and bone marrow induced by long-term estogen administration.

Pituitary weight, mitotic index and chromosomes were studied in male rats following a single or repeated dose of estradiol-benzoate for a total period of 210 days. Estrogen-induced pituitary hyperplasy eventually resulted in large pituitary tumors in some animals. The mitotic index increased until day 90, when it diminished, with chromosomes partly replaced by chromatin clusters. Most of the cells of the hyperplastic pituitaries maintained a normal diploid karyotype. However, a limited number of abnormal stem-lines with marker chromosomes appeared at a relatively early stage of the hyperplastic reaction of the pituitary. Later the tumors were characterized by an increase of number of aneuploid cells. In the bone marrow estrogens significantly lowered the mitotic index without any detectable change in chromosomal morphology.

Aneuploidy↗
PubMed1976

Dopaminergic control of adenohypophysial weight and serum ceruloplasmin level in rats.

Twice a week male rats were given injections of 1 mg estradiol benzoate as an aqueous microcrystalline suspension; they were also given 0.1, 0.2 or 0.4 mg Pimozide (a dopamine receptor blocker) daily in their food. Only the maximum Pimozide dose potentiated the effect of estradiol on adenohypophysial weight and on the binding capacity of adenohypophysial proteins for thyroxine in vitro. The estrogen-induced increase in the serum ceruloplasmin level, however, was potentiated significantly by all 3 Pimozide doses.

Animals↗
PubMed1976

[Ceruloplasmin].

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Adrenocorticotropic Hormone↗
PubMed1976

Specificity of the interation of thyroxine with rat adenohypophyseal proteins.

The proportion of thyroxine specifically bound to the proteins of the control and the oestrogenized rat adenohypophysis was estimated by determining the rate of ligand exchange, which was found to be higher in the oestrogenized adenohypophysis. The dissociation constants of this interaction were determined by analyzing saturation of the binding proteins with mounting labelled thyroxine concentrations and with a mixture of labelled and unlabelled thyroxine, using the equilibrium-maintaining batchwise Amberlite method. K(dis) for the interaction of thyroxine with the proteins of the control adenohypophysis was 6 X 10(-8) M and K(dis) for its interaction with the proteins of the oestrogenized adenohypophysis was 2.5 X 10(-8) M (i.e., 2.4 times lower). The maximum binding site concentrations were 1.05 X 10(-11) mol/mg. protein for the control adenohypophyses and 0.625 X 10(-11) mol/mg. protein for the oestrogenized adenohypophyses (i.e., 60% of the control value). Oestrogenization probably primarily stimulates the synthesis of specific thyroxine receptors in the rat adenohypophysis.

Animals↗
PubMed1975

[Association of thyroxine with subcellular fractions of rat liver and adenohypophysis in vitro (author's transl)].

After incubation of thyroxine (T4) labelled with 125I with liver and adenohypophysial homogenate and differential centrifuging into the "nuclear" fraction (600 g), "mitochondrial" (10 000 g), "microsomal" (105 000 g) fraction and cytosol the authors found a marked preference of association of T4 with mitochondria of rat adenohypophyses; the mitochondrial fraction of rat liver was not preferred. The effect of oestrogens was manifested in addition to the usual increase in weight of the adenohypophysis by increased binding of thyroxine with proteins of adenohypophysial mitochondria of oestrogen-treated animals. In liver this effect was lacking. Subfractionation of mitochondria into a membranous and soluble fraction revealed that a preferential association of thyroxine with membrane proteins of pituitary and liver mitochondria develops, the amount of T4 association protein (per protein unit) was several times (3-6x) higher in membrane proteins, as compared with soluble proteins.

Animals↗
PubMed1975

Inhibition of thyroxine binding to adenohypophysial proteins in vitro by 2,4-dinitrophenol administered in vivo.

Male and female rats were given oestradiol benzoate (1 mg as a microcrystal aqueous suspension i.m. twice a week), 0.0033% 2.4-dinitrophenol (DNP) in their food (about 1 mg/rat/day), or 0.1% DNP in their food (about 30 mg/rat/day), or both oestradiol and DNP. The smaller DNP dose mildly stimulated food consumption and did not affect body weight. The larger dose strongly inhibited food consumption in the first two weeks of the experiment; consumption then returned to the control level, but body weight fell markedly at the same time. After 3 weeks' administration of both the small and the large dose of DNP, adrenal weight in the males was raised and the weight of the gonads was unchanged. The large DNP dose severely reduced the weight of the seminal vesicles and the uteri. It also inhibited the accumulation of radioiodine in the thyroid of both males and females. Isolated administration of the oestrogen raised adrenal weight in the males and ovarian and uterine weight in the females; it reduced the weight of the testes and seminal vesicles. These reactions were not affected by DNP. A pronounced oestradiol-induced increase in the weight of the adenohypophyses was accompanied by raised thyroxine binding to the adenohypophysial proteins in vitro. DNP inhibited the growth reaction of the adenohypophysis to the oestrogen only slightly and non-significantly, but significantly inhibited the thyroxine binding reaction to the adenohypophysial proteins in vitro. By itself, DNP had no effect on adenohypophysial weight, but reduced thyroxine binding to the adenohypophysial proteins in vitro, especially in males. The effect of DNP was similar to that of thyroxine observed in earlier experiments; nothing is known of its mechanism.

Adrenal Glands↗