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Biomedical subjects

L Gabriel

Publications and source records attributed to L Gabriel.

At least 37 records · Page 2Linked to original sources
PubMed1986

Methylglyoxal-tubulin interaction: studies on the aldehyde effects on hepatoma, liver and purified microtubular protein.

Methylglyoxal antiproliferative action is well known; this action may be exerted by a non-enzymic mechanism and may directly involve the microtubular system. Our purpose was to verify this hypothesis, by studying the aldehyde effect on normal and tumour microtubular protein. Methylglyoxal incubation of normal and tumour liver cell homogenates causes inhibition of colchicine binding activity above all at higher concentrations. The aldehyde administration to the purified microtubular protein induces alterations in some tubulin properties already at lower concentrations. These results show a possible tubulin-methylglyoxal interaction, also if the reaction mechanism is so far unclear.

Aldehydes↗
PubMed1985

4-Hydroxy-alkenals interaction with purified microtubular protein.

4-Hydroxy-alkenals effect on microtubular system has been investigated, comparing the activity of both biogenic and non-biogenic aldehydes. As these aldehydes react essentially with sulphydryl groups, their action on titratable thiol groups microtubular protein was studied. These compounds evidenced an inhibitory effect on this parameter and on tubulin polymerization, where sulphydryls are essential. 4-Hydroxy-alkenals inhibit tubulin polymerization in a dose-dependent manner (0.1-1 mM), with the exception of 4-hydroxy-octenal, that shows an inhibitory action only in concentrations from 0.5 mM up. Its behaviour is very anomalous: in fact the tubulin-colchicine binding, is stimulated rather than inhibited, whereas such binding is inhibited by the other tested aldehydes. Our present results give then a support for an interaction between 4-hydroxy-alkenals and microtubular protein.

Aldehydes↗
PubMed1985

Intraoperative adjustment of eye muscle surgery. Correction based on eye position during general anesthesia.

During general anesthesia, the eye position of patients with strabismus, measured by Krimsky's test at 1 m, 30 minutes after induction, has a linear correlation with the eye position measured clinically preoperatively. A similar study was performed on 77 patients; however, Hirschberg's test was used for simplicity and was performed as soon as the patient was in a surgical plane of anesthesia. We confirmed that there was a linear correlation. We also adjusted the surgery performed in seven cases where the test was anomalous, ie, when the eye position under anesthesia was more than 15 prism diopters more or less than expected based on preoperative clinical measurements. We did approximately 1 mm more or less surgery than we had planned on each eye muscle. This significantly improved the final results in anomalous cases. Patients with anomalous tests who did not have such adjustments had significantly poorer results.

Adolescent↗
PubMed1985

Multiple myeloma with crystalline inclusions in most hemopoietic cells.

Intracytoplasmic inclusions were observed at light and electron microscopy in the cells of most of the hemopoietic series, including erythroblasts, in a case of multiple myeloma IgG kappa. The inclusions were of crystalline nature, surrounded by smooth membrane. An indirect immunoperoxidase method on thick sections confirmed their immunoglobulin G kappa nature. The fact that crystals were observed in various hemopoietic series suggests that, except for the plasma cells, their presence is more likely due to phagocytosis than to synthesis and, therefore, that they are not a clone marker.

Aged↗
PubMed1985

Effect of methylglyoxal on tumour microtubular protein.

Methylglyoxal inhibits cell division, exerting an antiproliferative action on tumour cells. Supernatants from ascites hepatoma cell homogenate, previously incubated with the aldehyde, showed a decrease in colchicine binding activity dependent on methylglyoxal concentration. In contrast, in vivo treatment of tumour-bearing rats apparently did not cause a significant impairment of microtubular protein, suggesting that the aldehyde interaction with microtubules cannot be considered responsible for its carcinostatic action.

Aldehydes↗
PubMed1984

Effect of lipid peroxidation on microtubular protein.

CCl4 and ADP-Fe3+ determine an increased microsomal lipid peroxidation in liver tissue which is related to an impairment of the tubulin molecule in the case of CCl4 while no alteration is evident with ADP-Fe3+. Such difference could be explained in terms of different intermediate or end products towards which the tubulin molecule shows a different susceptibility.

Adenosine Diphosphate↗
PubMed1982

Control of cell protein catabolism in rat liver. Effects of starvation and administration of cycloheximide.

1. The loss of liver protein occurring in rats starved for 24 h was largely prevented by the administration of repeated doses of cycloheximide, an inhibitor of protein synthesis. Similar effects were produced on tubulin, a 'fixed' liver protein. 2. Starvation accelerated, whereas cycloheximide markedly lowered, the rate of protein radioactivity decay after labelling with [3H]valine or [14C]bicarbonate, indicating that changes in catabolic rates played an important role in the above regulations of liver protein mass. 3. The total activity of several lysosomal hydrolases showed little change in livers of starved rats, but a marked progressive decline developed after the administration of cycloheximide, particularly in the activities of cathepsins B, D and L as well as acid ribonuclease. There was no evidence that these changes might be due to endogenous inhibitors (at least for cathepsin B activity, which fell to less than 30% of the control values) or enzyme leakage into the bloodstream; rather, plasma beta-galactosidase and beta-N-acetylglucosaminidase activities fell progressively during the cycloheximide treatment. 4. Endogenous proteolytic rates, measured in vitro by incubating subcellular preparations from livers prelabelled in vivo with [3H]valine, were markedly decreased in cycloheximide-treated animals. 5. The osmotic fragility of hepatic lysosomes, appreciably enhanced in starved animals, after cycloheximide treatment was found to be even lower than in fed controls. 6. The present data are consistent with the view that in starved animals the loss of liver protein is mostly accounted for by increased breakdown, due, in part at least, to enhanced autophagocytosis. 7. Cycloheximide largely counteracted these effects of starvation, altering the liver from being 'poised' in a proteolytic direction to a protein-sparing condition. The present data suggest that, besides suppression of the autophagic processes, a decrease in the lysosomal proteolytic enzyme system may also play a role in this regulation, and they seem to provide further circumstantial evidence for the existence of co-ordinating mechanisms between protein synthesis and degradation.

Animals↗
PubMed1982

Intestinal phospholipase A and triglyceride lipase: localization and effect of fasting.

We investigated the distribution of phospholipase A and triglyceride lipase in the rat small intestine and the effects of heparin and hormones on enzyme release. Phospholipase A activity was 10 times higher in the ileum than in the jejunum; triglyceride lipase activity was threefold higher in the jejunum than in the ileum. Activities of both enzymes were much greater in villus than in crypt cells. The specific activity of phospholipase A was highest in microsomes and least in cytosol. The crude nuclei and brush-border fraction contained 40.5% of total phospholipase A activity; mitochondria contained 33.8%; and microsomes, 17.4%. Phospholipase A activity increased significantly in the distal intestinal mucosa in fasted rats compared with controls. Heparin did not increase the release of phospholipase A by isolated intestinal cells or perfused intestinal vasculature. Thus, the small intestine probably does not contribute significantly to the phospholipase A activity of postheparin plasma. Hormones and cAMP, which inhibit the secretion of phospholipase A and triglyceride lipase from isolated hepatocytes, had no effect on the release of either enzyme from intestinal cells.

Alkaline Phosphatase↗
PubMed1981

[Frequency of HLA antigens in Greek patients with open-angle glaucoma].

50 Greek patients with primary open-angle glaucoma were tissue-typed for a total of 29 HLA antigens (groups A and B). The results were compared with those of 200 control persons. A statistically significant difference at the level of p less than 0.05 was noted only with regard to the A2 antigen. These findings are in accordance with those of other authors who found no correlation between glaucoma simplex and the frequency of HLA antigens.

Adult↗
PubMed1978

Ethanol-induced hepatotoxicity; experimental observations on the role of lipid peroxidation.

Hepatic lipid peroxidation in vivo or in vitro as measured by UV absorption spectra of microsomal lipids or by production of TBA-reacting substances by whole liver homogenates, was studied after acute or during prolonged administration of ethanol. No evidence of peroxidative derangement of liver microsomal lipids in vivo was detected in either experimental situation, while the production of TBA-reacting substances by pooled liver homogenates incubated in vitro appeared slightly increased. Treatment with reduced glutathione (GSH and 2-mercaptopropionylglycine (2-MPG) was able to reduce fatty liver in acute and prolonged ethanol dosing, as well as the production of TBA-reacting compounds. Similar effects were obtained with 3-amino-1,2,4-triazole which was assayed only in acute experiments. By contrast, hepatic triglyceride accumulation induced by a single intoxicating dose of ethanol was not affected by preventive treatment with pyrazole which seemed to act as a pro-oxidant agent as far as the production of TBA-reacting substances is concerned. The role of lipid peroxidation as a pathogenic mechanism for acute and chronic ethanol-induced hepatotoxicity is discussed in relation to the action of anti-oxidant compounds which are active in preventing liver injury. It is concluded that lipid peroxidation is unlikely to be an important mechanism in alcohol hepatotoxicity.

Animals↗