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Biomedical subjects

P Arslan

Publications and source records attributed to P Arslan.

34 records · Page 2Linked to original sources

Nuclear membrane-staining antinuclear antibody in patients with primary biliary cirrhosis.

An antinuclear antibody specific for nuclear membrane (ANMA) was observed by the immunofluorescence method in sera from patients with primary biliary cirrhosis (PBC). ANMA was present in 18 of 63 PBC sera (28.5) and in 1 of 431 control sera (0.2%). Its reaction appeared as a thin fluorescent ring confined to the nuclear envelope and was more evident when the sera were highly diluted and the fluorescence, due to frequently associated antimitochondrial antibody, faded. The ANMA fluorescent pattern was confirmed by indirect immunoperoxidase staining. ANMA was seen on both tissue cryostat sections and HEp-2 cells. It was a poorly or non-complement-fixing IgG, specific for an antigen resistant to DNase I, RNase, and trypsin. The significance of its presence in PBC in unknown at present. Identification of its antigen with one of the centromeric antigens is suggested.

Animals↗

Effects of chromium(VI) and chromium(III) on energy charge and oxygen consumption in rat thymocytes.

The cytotoxic effects of chromium compounds in two oxidation states have been studied in rat thymocytes. endogenous nucleotide levels and oxygen consumption were examined as relevant parameters of the physiological state of the cell. Incubation of rat thymocytes with Cr(VI) produced a marked unbalance of endogenous purine nucleotide pool and a parallel decrease in oxygen consumption. A close correlation between the reduction of oxygen consumption and ATP level in rat thymocytes treated with increasing concentrations of Cr(VI) has been found. In rat thymocytes permeabilized with digitonin and in isolated rat liver mitochondria both Cr(VI) and Cr(III) showed, at different range of concentrations, a marked inhibition of maximal oxygen consumption rate (uncoupled respiration). The effects observed were depending on chromium oxidation state and on different mitochondrial sites of substrate oxidation.

Adenosine Diphosphate↗

Effects of a met-enkephalin analogue on motility, O2 consumption, and ATP content of human spermatozoa.

Opioid narcotics are present in seminal plasma, although their physiological effect on spermatozoa is still unknown. This study reports data on metabolic parameters of human spermatozoa in the presence of a met-enkephalin analogue: D-Ala2-Mephe4-Met-(o)-ol-Enkephalin, FK 33824, Sandoz, Basel, Switzerland (DAMME), and its receptor antagonist naloxone hydrochloride, Endo Laboratories, Garden City, New York. Our findings indicate that the metenkephalin analogue reduces sperm motility and cellular O2 consumption without affecting cellular ATP content and viability. The hypothesis that DAMME acts on adenylate-cyclase is briefly discussed.

Adenosine Triphosphate↗

cis-Unsaturated fatty acids uncouple mitochondria and stimulate glycolysis in intact lymphocytes.

In intact lymphocytes, linoleic acid acts as a typical mitochondrial uncoupler: it substantially decreases the mitochondrial membrane potential and the cellular ATP level, while stimulating oxygen consumption and glycolysis. Under these conditions the inhibition of cellular functions by linoleic acid cannot be attributed to its postulated effects on lipid domains in the plasma membrane.

Adenosine Triphosphate↗

Effect of ionophores on lymphocyte cellular metabolism.

The effect of valinomycin, nigericin, gramicidin S and D, A23187 and X537A on respiration and cellular ATP content of rat spleen lymphocytes is presented. It has been found that while valinomycin and nigericin interfere with mitochondrial functions gramicidin D does not show an appreciable effect. These results are explained in terms of different ability of ionophores to re-distribute among intracellular membranes. A23187 and X537A, added with Ca2+, strongly enhanced O2 consumption and reduced cellular ATP content.

Animals↗

Anti-immunoglobulin, cytoplasmic free calcium, and capping in B lymphocytes.

This paper examines, in mouse spleen lymphocytes, the effect of anti-immunoglobulin (anti-Ig) on the cytoplasmic free calcium concentration, [Ca2+]i, measured with the fluorescent indicator quin2, and the relationship of [Ca2+]i to the capping of surface Ig. Anti-Ig causes a rapid rise of [Ca2+], which precedes capping. Assuming that only those 40-50% of the cells which can bind anti-Ig (the B cells) undergo a [Ca2+]i response, [Ca2+]i in those cells approaches 500 nM. It declines to resting levels over many minutes, roughly paralleling the formation of caps. Part of the [Ca2+]i signal is due to stimulated influx across the plasma membrane, since in Ca2+-free medium, anti-Ig gives a smaller and shorter [Ca2+]i rise. The amplitude of this reduced transient now varies inversely with quin2 content, as if some 0.25 mmol Ca per liter of cells was released into the cytoplasm from internal stores. These stores are probably sequestered in organelles since A23187 in Ca2+-free medium also causes a transient [Ca2+]i rise after which anti-Ig has no effect. These organelles seem not to be mitochondria because uncouplers have hardly any effect on [Ca2+]i. Though anti-Ig normally raises [Ca2+]i before causing capping, there seems to be no causal link between the two events. Cells in Ca2+-free medium whose stores have been emptied by A23187, still cap with anti-Ig even though there is no [Ca2+]i rise. Cells loaded with quin2 in the absence of external Ca2+ still cap anti-Ig normally even though their [Ca2+]i remains steady at below 30 nM, four times lower than normal resting [Ca2+]i.

Adenosine Triphosphate↗

Effect of monovalent cation ionophores on lymphocyte cellular metabolism.

The effect of valinomycin, nigericin and gramicidin on the cellular O2 consumption and on ATP content has been investigation. It has been found that while valinomycin and nigericin interfere with mitochondrial functions, gramicidin D does not show any appreciable effect. These results are explained in terms of the differing abilities of ionophores to redistribute among intracellular membranes.

Adenosine Triphosphate↗

Phospholipid release from sonicated vesicles induced by a "critical" fatty acid concentration.

Dipalmitoyl phosphatidylcholine vesicles incubated in the presence of increasing amounts of myristic acid showed a progressive translocation of phospholipid molecules across a dialysis membrane. The rate of phospholipid translocation increased abruptly at a 'critical' value of myristic acid concentrations. The translocation rate of mixed dipalmitoyl phosphatidylcholine/myristic acid vesicles obtained by cosonicating the two components was also dependent on a 'critical' fatty acid concentration. A marked release of K+ and different responses of fluorescent probes to the fatty acid addition were observed at this concentration.

Chromatography, Gel↗

Phospholipid exchange and size enlargement in sonicated vesicles induced by a 'critical' fatty acid concentration.

Size enlargement of dipalmitoyl phosphatidylcholine vesicles was greatly accelerated in the range of the phase-transition temperatures, when fatty acid concentration was above a threshold level ('critical' concentration). This 'critical' concentration varied with the length of the fatty acid chain. The size enlargement process had second-order kinetics dependent on the vesicle concentration. Alkaline pH and low ionic strength inhibited the rate of size enlargement. Phospholipid exchange between dimyristoyl and dipalmitoyl phosphatidyl-choline vesicles increased abruptly above a 'critical' fatty acid concentration. The donor vesicles were those vesicles in which fatty acids reached the 'critical' concentration. The phospholipid exchange occurred both in fluid- and in solidstate vesicles. The 'critical' fatty acid concentration accelerating the phospholipid exchange process was lower than that accelerating the size enlargement process. The phospholipid exchange process explained in terms of a diminished hydrophobic attraction among the phospholipid molecules of the bilayer occurs via a free phospholipid molecule transfer through the aqueous phase. The size enlargement process is interpreted in terms of high fatty acid concentration in the membrane fluid domains. The membrane structure is locally perturbed inducing vesicle sticking after collision.

Fatty Acids↗

Labelling of cardiolipin in vitro.

A method for labelling the polar head groups of cardiolipin is described. Labelling was carried out on sonicated cardiolipin/water suspensions. The free hydroxyl group of cardiolipin was oxidised with an excess of p-(diazonium) benzenesulfonic acid (DABS) and then reduced with NaB3H4. Isopropanol was oxidised in the presence of DABS to test the reactivity of the diazonium salts, and the reaction product was analysed by means of gas-chromatography. Labelled cardiolipin, identified by thin-layer chromatography (TLC), was chromatographically pure and identical to untreated cardiolipin. The hydrolysis of cardiolipin confirmed that the labelling was at the level of polar head groups.

Cardiolipins↗

Proton electrochemical gradient and phosphate potential in submitochondrial particles.

The aerobic uptake of inorganic ions, such as 86Rb+ or 125I-, by submitochondrial particles, is about one order of magnitude lower than the uptake of organic ions, such as acridines or 8-anilino-1-naphthalene sulphonate. The values of deltapH, the transmembrane pH differential, and deltapsi, the transmembrane membrane potential are between 60 and 100 mV when calculated on the inorganic ions and between 150 and 240 mV when calculated on the organic ions. The discrepancy between the deltapH and deltapsi values from organic and inorganic ions is large at high but not at low ion/protein ratios. 2. In the absence of weak bases and strong acids the values of deltamuH, the proton electrochemical potential difference, are close to 100 mV and the magnitude of deltapH and deltapsi are similar. Weak bases decrease deltapH and enhance deltapsi. Strong acids decrease deltapsi and enhance deltapH. Interchangeability of deltapH with deltapsi occurs at low concentrations of weak bases and strong acids. High concentrations of weak bases and strong acids cause depression of deltamuH. 3. Concentrations of weak bases capable of abolishing deltapH, do not affect ATP synthesis. Concentrations of strong acids capable of abolishing deltapsi affect only slightly ATP synthesis. Concentrations of weak bases and strong acids capable of causing a decline of deltapH + deltapsi inhibit ATP synthesis. 4. Depression of deltamuH is paralleled by inhibition of ATP synthesis and decline of deltaGp, the phosphate potential. Abolition of ATP synthesis occurs only when deltamuH is below 20 mV. The deltaGp/deltamuH ratio increases hyperbolically with the decrease of deltamuH.

Acridines↗

Dark and photohemolysis of erythrocytes by furocoumarins.

It has been shown that various furocoumarins are able to cause dark hemolysis in red blood cells (RBC). However, this effect is evident only at relatively high furocoumarin concentrations (4.6 x 10(-4) M) - much higher than those used in photosensitization experiments or photochemotherapeutic treatments. Among the various furocoumarins examined in this study, only psoralen (Ps) and 3-carbethoxypsoralen (3-CPs) showed strong photohemolytic effects, while the other compounds revealed little or no activity. This fact indicates that Ps and 3-CPs are able to induce selective damage to the cell membrane of RBC. By pre-irradiating furocoumarin in ethanol or isotonic saline solutions and adding the irradiated solutions to a RBC suspension, hemolysis was observed in various compounds. The products of photolysis which form during pre-irradiation may be responsible, in terms of hemolysis, for toxic effects on RBC.

Darkness↗

[Leukotriene B4 in gastritis and peptic ulcer].

To contribute to a better understanding of the role of leukotrienes in inflammatory conditions of the upper gastrointestinal tract, leukotriene B4 (LTB4) levels were measured by specific radioimmunoassay in extracts of mucosal biopsies from the stomach and duodenum of control subjects and of patients with gastritis, benign gastric ulcer and duodenal ulcer. The control mucosa contained measurable levels of LTB4. Levels were 20% higher in gastritis than in controls and the lowest levels were found in the patients with no bile reflux. LTB4 levels were more than 3 times higher in duodenal ulcer (p less than 0.025) than in controls, whereas gastric ulcer margins had very low levels. No clear relationship was found between LTB4 levels and the drugs used in treatment. While these data do not explain the role of LTB4, they suggest that LTB4 may be an important mediator of the inflammation accompanying or leading to development of duodenal ulcer.

Analysis of Variance↗