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Biomedical subjects

S Malamed

Publications and source records attributed to S Malamed.

49 records · Page 3Linked to original sources
PubMed1979

Acute self-suppression of corticosteroidogenesis in isolated adrenocortical cells.

The relation between steroidogenesis induced by ACTH and that induced by exogenous concentrations of glucocorticoids was studied in isolated adrenocortical cells. Exogenous corticosterone and cortisol, in concentrations within the production capacity of the adrenal gland, suppressed steroidogenesis induced by ACTH in rat and beef cells, respectively. The precursors pregnenolone and progesterone enhanced steroidogenesis in both rat and beef cells. Aldosterone in rat cells and 17 beta-estradiol in rat and beef cells had little if any effect on steroidogenesis. Either suppression or stimulation by exogenous steroids was acute, that is, after 2-h incubation for rat cells and 1-h incubation for beef cells. A direct suppressive action of end product glucocorticoids is indicated. This observed self-suppression of adrenocortical cells suggests the existence of a mechanism for the find adjustment of steroidogenesis that operates in addition to the classical control exerted by the anterior pituitary.

Adrenal Cortex↗
PubMed1975

Acute effects of ACTH on dissociated adrenocortical cells: quantitative changes in mitochondria and lipid droplets.

To study the role of certain organelles in steroidogenesis, dissociated rat adrenocortical cells were incubated for two hours with ACTH at a concentration that induces a high level of steroid production. Sections of ACTH treated and untreated cells were photographed in the electron microscope, and morphometric analysis was undertaken to assess possible ACTH-induced changes in total cell volume, volume density and numerical denisty of lipid droplets and mitochondria. There was no change in total cell volume. Lipid droplet volume density and numerical density decreased. Mitochondrial volume density did not change, but numerical density increased. The decrease in lipid droplet volume density indicates a rapid depletion of cholesterol for steroid production. This depletion is almost entirely due to the disappearance of lipid droplets, rather than to an overall diminution in their size, as shown by the decrease in lipid droplet numerical density. The mitochondrial data suggest that the adrenocortical cell has an adedquate mitochondrial apparatus to respond to acute ACTH stimulation with increased steroid output without an increase inmitochondrial volume.

Adrenal Cortex↗
PubMed1975

The hypothalamo-neurohypophysial complex in organ culture: effects of metabolic inhibitors, biologic and pharmacologic agents.

Organ cultures of the guinea pig hypothalamo-neurohypophysial complex synthesize the octapeptide hormone, vasopressin, a specific product of the neurosecretory cells of the supraoptic nucleus. Inhibitors of both protein and RNA synthesis (cycloheximide and bromotubercidin respectively) were found to block vasopressin biosynthesis. In the presence of bromotubercidin, the apparent half-time of decline in the rate of hormone biosynthesis was about 28 h. Colchicine inhibited the distal transport of vasopressin into the posterior pituitary. Ultrastructural studies on colchicine-treated cultures indicated the neuronal stalks were intact and that neurotubules were still present. The narcotic drug, levorphanol at 10-7 M and 10-9 M was found to inhibit RNA synthesis by 20 percent. At these concentrations it had no demonstrable effect on vasopressin synthesis. Cultures established from animals that had been rendered tolerant to narcotics also had no observable alterations in vasopressin biosynthesis, although the initial pituitary vasopressin content of these cultures was reduced by about 35 percent. Various pharmacologic and biologic compounds were tested for their effects on vasopressin biosynthesis in organ cultures. Dibutyryl cyclic AMP, estradiol-17beta, nicotine, nerve growth factor (NGF), and pineal extract all had no effects under the present experimental regimen. Medium conditioned by the presence of fetal hypothalami of 40-55 days gestation produced a 2-4 fold increase in vasopressin biosynthesis in cultures established from adult animals. Medium conditioned by fetal cerebral cortex, liver, or hypothalamic tissue from fetuses of less than 33 days gestation did not have this stimulatory effect.

Antibiotics, Antineoplastic↗
PubMed1965

The effect of calcium withdrawal on the structure and function of the toad bladder.

Previous reports have indicated that calcium is necessary to support active sodium transport by the toad bladder, and may be required as well in the action of vasopressin on both toad bladder and frog skin. The structure and function of the toad bladder has been studied in the absence of calcium, and a reinterpretation of the previous findings now appears possible. When calcium is withdrawn from the bathing medium, epithelial cells detach from one another and eventually from their supporting tissue. The short-circuit current (the conventional means of determining active sodium transport) falls to zero, and vasopressin fails to exert its usual effect on short-circuit current and water permeability. However, employing an indirect method for the estimation of sodium transport (oxygen consumption), it is possible to show that vasopressin exerts its usual effect on Q(oo2) when sodium is present in the bathing medium. Hence, it appears that the epithelial cells maintain active sodium transport when calcium is rigorously excluded from the bathing medium, and continue to respond to vasopressin. The failure of conventional techniques to show this can be attributed to the structural alterations in the epithelial layer in the absence of calcium. These findings may provide a model for the physiologic action of calcium in epithelia such as the renal tubule.

Animals↗