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Biomedical subjects

L Gabriel

Publications and source records attributed to L Gabriel.

At least 55 records · Page 3Linked to original sources
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↗
PubMed1977

Inhibition of colchicine binding to rat liver tubulin by aldehydes and by linoleic acid hydroperoxide.

The onset of fat accumulation within CCl4 poisoned hepatocytes, occurring as early as 1 h after treatment, is known to be provoked by a block in lipoprotein secretion. Lipoprotein secretion involves the function of the microtubular system. Several data indicate that this early block in lipoprotein secretion is not primarily the consequence of impaired protein synthesis. Therefore effects of some derivatives of lipid peroxidation, i.e. aldehydes and linoleic acid hydroperoxide were investigated. The results described in this paper shown that the above mentioned lipid peroxidation derivatives inhibit, with different activities, [3H] colchicine binding to liver high-speed supernates. Percentage binding inhibition is directly related to concentrations of aldehydes of LAHPO. LAHPO is more effective than aldehydes. Among the aldehydes tested, 4-hydroxypentenal, produced during lipid peroxidation of biological materials, was the most active. The presence of thiols, added to the incubation medium, partially protects against the inhibition of [3H] colchicine binding by aldehydes. This suggests that aldehydes act by reacting with -SH groups of tubulin. The possibility that interaction between lipoperoxidation derivatives and tubulin in vivo may contribute to the onset of fat infiltration in CCl4 poisoning is discussed.

Aldehydes↗
PubMed1977

"Acute" granulomatous pericarditis. clinical and hemodynamic correlate.

Ten cases of acute constrictive pericarditis from southern Iran are presented. They differed from chronic constrictive pericarditis by the absence of ascutes and edema of the lower extremities, the presence of cardiomegaly on posteroanterior chest x-ray film, the lack of calcification of the pericardium on fluoroscopic examination, and the presence of sinus rhythm in all cases. If tuberculosis is the etiologic agent, early pericardiectomy should be considered. This is especially important in areas where close follow-up of patients is difficult or impossible, since all patients in this series ultimately developed clinically significant constriction.

Adolescent↗
PubMed1975

Effect of cholesterol content on some physical and functional properties of mitochondria isolated from adult rat liver, fetal liver, cholesterol-enriched liver and hepatomas AH-130, 3924A and 5123.

The cholesterol to phospholipid ratio in mitochondria from hepatomas AH-130, 3924A and 5123 is higher than in the particles isolated from adult or fetal rat livers. Nearly all the cholesterol of hepatoma mitochondria is located in membranes. As in liver mitochondria, in the particles isolated from hepatoma AH-130 there is more cholesterol in the outer than in the inner membrane. In mitochondria from cholesterol-enriched liver and hepatomas, there occurs a decrease in extent of hypoosmotic and phosphate-induced swelling and a decrease of conformational changes linked to energy states. The phenomenon is more marked in particles which exhibit higher cholesterol to phospholipid ratios. A statistically significant negative correlation exists between the cholesterol to phospholipid ratio and extent of volume or conformational changes. No significant modifications of these parameters were found in fetal liver mitochondria. Cholesterol content does not influence K+ uptake by cholesterol-enriched or hepatoma mitochondria. Nor does cholesterol content affect the respiratory increment related to this uptake. As a consequence of K+ uptake, total mitochondrial water exchangeable with tritiated water rises 20% while sucrose-impermeable water rises 42-48% in both adult rat liver and hepatoma AH-130 mitochondria. Absorbance changes linked to ion uptake do not correspond merely to variations in mitochondrial water content. Water content is apparently not influenced by the cholesterol to phospholipid ratio. However, the ratio is significantly correlated to both extent and initial rate of absorbance decrease of mitochondrial suspensions during K+ uptake. The higher the ratio, the lower the extent and initial rate of absorbance decrease.

Animals↗
PubMed1975

Functional and structural alterations of liver ergastoplasmic membranes during DL-ethionine hepatocarcinogenesis.

Different functional and structural properties of rat liver microsomes were studied during hepatocarcinogenesis induced by 0.25% DL-ethionine. During the first to fourth months of ethionine feeding, great decreases of cytochrome P-450 content, reduced nicotinamide adenine dinucleotide phosphate-dependent lipid peroxidation, and animopyrine demethylase activity occurred. No changes in the reduced nicotinamide adenine dinucleotide phosphate-cytochrome c reductase activity were observed. These functional alterations were paralleled by an increase in membrane-free ribosomes and by changes in the relative proportions of phospholipid fatty acids in microsomes. After the end of ethionine feeding, when hyperplastic nodules and/or hepatomas were present, the above functional and structural parameters were studied in the latter tissues, as well as in surrounding nonodular liver. Decreases in cytochrome P-450 content, lipid peroxidation, and animopyrine demethylase activity were documented in hyperplastic nodules and hepatomas. In hepatomas, the alterations were more marked and decrease of reduced nicotinamide adenine dinucleotide phosphate-cytochrome c reductase activity was also found. All these functional parameters were quite normal in surrounding nonnodular liver. Similarly, alterations in phospholipid fatty acid composition disappeared in surrounding nonnodular liver, but they partially persisted in both hyperplastic nodules and hepatomas. In contrast, the increase in membrane-free ribosomes also occurred in surrounding nonnodular liver, although to a lower extent than in hyperplastic nodules and hepatomas. These data are discussed in relation to the problem of the cellular precursors of hepatomas.

Animals↗