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Biomedical subjects

D Romeo

Publications and source records attributed to D Romeo.

At least 91 records · Page 5Linked to original sources
PubMed1977

Effect of intraamniotic administration of vitamin A on rat fetuses.

The present study examines the effect of intraamniotic (i/a) administration of vitamin A to rat fetuses. Vitamin A aquasol in concentrations of 50 I.U., 100 I.U., and 300 I.U., was mixed in 5 microliter of saline. On day 13 of gestation, each of the tree experimental subgroups were injected i/a with varying doses of vitamin A. The four control subgroups consisted of: (1) i/a injection of 5 microliter of saline only, (2) amniotic puncture only, (3) laparotomy or (4) i/a injection of sorethytan oleate. The fetuses were recovered on day 18 of gestation, and were weighed and examined for gross malformations. The viable fetuses from the experimental groups showed various malformations such as cleft palate, micrognathia and limb defects. The percentage of resorbed fetuses was significantly high. The control fetuses showed a moderate number of resorptions; however the percentage of malformations was small. The results show that the i/a method can be used effectively to study the direct teratogenic effect of vitamin A on the fetuses.

Abnormalities, Drug-Induced↗
PubMed1976

The dissociation of exocytosis and respiratory stimulation in leucocytes by ionophores.

By exploiting the unique characteristics of three ionophores, experimental conditions were found which permit the dissociation of respiratory stimulation from secretion in polymorphonuclear leucocytes. A marked stimulation of respiration was produced by ionophore X537A, which binds and transports both alkali-earth and alkali cations. The stimulatory activity of this ionophore was the same at either high or low Na+/K+ ratios in the medium and was virtually unaffected by extracellular Ca2+. A slight stimulation of oxygen consumption was also caused by the K+-selective ionophore valinomycin and by ionophore A23187, which complexes and transfers bivalent cations. Ionophore X537A and valinomycin were unable to stimulate selective release of granuleassociated beta-glucuronidase and gradually increased cell fragility, as monitored by increased leakage of lactate dehydrogenase. Ionophore A23187 slightly increased exocytosis of beta-glucuronidase. In a Mg2+-free medium, Ca2+, added simultaneously with ionophore A23187, greatly enhanced respiration and secretion of the granule enzyme. If Ca2+ was added a few minutes after the ionophore, exocytosis occurred, but no respiratory burst was observed. If the latter experiment was repeated in the presence of extracellular Mg2+, both secretion and respiration were stimulated. This effect was not produced by Mn2+ or Ba2+. It is proposed that Ca2+ is required for triggering selective secretion of granule enzymes from leucocytes is caused by an intracellular redistribution of cations, which may invovle Mg2+-dependent mechanisms.

Animals↗
PubMed1976

Metabolic perturbation of the inflammatory cells.

An activation of the oxidative metabolism of phagocytes is a regular concomitant of phagocytosis as well as of other functions of these cells such as exocytosis, chemotactic locomotion, and immune-adherence. Several other substances, some of which may be found in the inflammatory site, are also able to stimulate the oxidative metabolism of phagocytes, for example phospholipases, antileucocyte antibodies, endotoxins, fatty acids, surfactants and fragments of complement. This paper deals with, (1) the molecular events occurring within the plasma membrane that trigger the stimulation of the oxidative metabolism. An experimental model is presented that involves redistribution of ions across the plasma membrane of leucocytes as the trigger of the stimulated respiration and exocytosis; (2) the intracellular localization of the enzymatic system that is the effector of the metabolic response. A scheme is proposed for the mechanism of this enzymatic system which accounts for the production of highly reactive compounds such as hydrogen peroxide, superoxide anion radical and hydroxyl radical during the metabolic activation of phagocytes.

Animals↗
PubMed1976

Antitumor activity of equinatoxin.

Equinatoxin, a highly basic protein extracted from Actinia equina, causes an increase in the survival time of mice bearing the ascitic form of Ehrlich carcinoma, whereas it has no effect on L1210 leukaemia. When tested for in vitro cytotoxicity by the dye exclusion test, it shows a potent activity on both tumour cell lines, with ED50 of a few ng/ml. Higher concentrations produce an extensive lysis of the cells. The cytotoxic effects of Equinatoxin are inhibited by phospholipids, thus suggesting that its mechanism of action may be related to interactions with lipids or other charged components of cell membrane. The observed lack of in vivo activity against L1210 leukaemia presumably is due to poor systemic absorption of the protein and/or neutralization by serum factors.

Animals↗
PubMed1976

Influence of E. COLI POLysaccharide on the interaction of E. coli K+ and K- with polymorphonuclear leukocytes in vitro.

Both a K+ strain and a K- strain of E. coli withstand phagocytic killing by polymorphonuclear leukocytes and do not stimulate the respiratory burst, that accompanies phagocytosis in these cells, as compared with E. coli J 53 which are extensively and rapidly killed and stimulate the respiration of leukocytes. Both K+ and K- E. coli become readily phagocytosable after removal of their polysaccharide by heat treatment and are able to stimulate oxygen consumption by PMN. Heat treated E. coli J 53 stimulate the oxygen uptake of PMN less than live E. coli J 53. The polysaccharide extracted from either K+ or K- E. coli inhibits both phagocytosis of and the respiration stimulated by all the three heat-treated strains used. Instead the polysaccharide extracted from the phagocytosable strain J 53 stimulates the oxygen consumption of PMN exposed to the heat treated K- strain or heat treated J 53 itself.

Animals↗
PubMed1975

Concanavalin A as a probe for studying the mechanism of metabolic stimulation of leukocytes.

The disruption of the molecular organization of the plasma membrane of leukocytes by phagocytosable particles, or by agents such as surfactants, antibodies, phospholipase C, fatty acids and chemotactic factors, leads to a stimulation of the phagocyte oxidative metabolism. Concanavalin A (Con A) has been used as a tool to study the mechanism of this metabolic regulation. The binding of Con A to the surface of polymorphonuclear leukocytes (PMNL) or macrophages produces a rapid enhancement of oxygen uptake and glucose oxidation through the hexose monophosphate pathway (HMP). This is explained by an activation of the granular NADPH oxidase, the key enzyme in the metabolic stimulation. The effect of Con A is not due to endocytosed lectin, since Con A covalently coupled to large sepharose beads still acts as stimulant. The metabolic changes caused by Con A are reversible. If, after the onset of stimulation, sugars with high affinity for Con A are added to the leukocyte suspension, the activity of granular NADPH oxidase and the rate of respiration and glucose oxidation return to their resting values. The metabolic burst, while partially supressed by treatment of PMNL with iodoacetate, sodium flouride and cytochalasin B, is slightly increased by colchicine. Con A induces a selective release of granular enzymes (beta-glucuronidase, peroxidase, alkaline phosphatase) from PMNL, whereas no leakage of cytoplasmic enzymes is observed. The enzyme release is inhibited by iodoacetate and by drugs known to increase cell levels of cyclic AMP. Based on a current view of the mode of interaction between Con A and cell surfaces, a model of the metabolic disruption of leukocytes is presented.

Animals↗
PubMed1975

Differential cell proliferation of embryonic rat palatal processes as determined by incorporation of tritiated thymidine.

The differential cellular proliferation of the palatal processes in the Wistar albino rat was studied utilizing tritiated thymidine labeling. 3HTdr was given to pregnant rats at 14, 15, 16, and 17 days of gestation. The animals were killed one hour after injection. The fetuses were removed and the heads were embedded, sectioned, and an autoradiographic technique utilized. The autoradiograms were examined microscopically and labeling indices for various areas and regions of the palatal processes were calculated. The findings revealed that the pattern of cellular activity of mesenchymal and epithelial cells changes in different areas and regions of the palatal processes with different stages of secondary palate development.

Animals↗