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Biomedical subjects

A Santos-Ruiz

Publications and source records attributed to A Santos-Ruiz.

At least 19 recordsLinked to original sources
PubMed1985

Effect of chronic ethanol or acetaldehyde on hepatic alcohol and aldehyde dehydrogenases, aminotransferases and glutamate dehydrogenase.

Ethanol or acetaldehyde orally administered (15% and 2% respectively in drinking water) to male Wistar rats for three months induced alterations in the main liver enzymes responsible for ethanol metabolism, aspartate and alanine aminotransferases and NAD glutamate dehydrogenase. Ethanol produced a significant decrease in the activity of soluble alcohol dehydrogenase, while acetaldehyde induced alterations both in soluble and mitochondrial aldehyde dehydrogenases: soluble activity was significantly higher than in the control and ethanol-treated groups, and mitochondrial activity was significantly diminished. Both soluble aspartate and alanine aminotransferases showed pronounced increases by the chronic effect of acetaldehyde, while mitochondrial activities were practically unchanged by the effect of ethanol or acetaldehyde. Mitochondrial NAD glutamate dehydrogenase showed a rise in its activity both by the effect of chronic ethanol and acetaldehyde consumption. The level of metabolites assayed in liver extracts showed marked differences between ethanol and acetaldehyde treatment which indicates that ethanol produced a remarkable increase in glutamate, aspartate and free ammonia together with marked decrease in pyruvate and 2-oxoglutarate concentrations. Acetaldehyde consumption induced a significant decrease in 2-oxoglutarate and pyruvate concentrations. These observations suggest that ethanol has an important effect on the urea cycle enzymes, while the effect of acetaldehyde contributes to the impairment of the citric acid cycle.

Acetaldehyde↗
PubMed1983

The effect of chronic ethanol administration on lipogenesis in liver and adipose tissue in the rat.

Rates of lipogenesis de novo have been studied in liver and epididymal fat pads of male rats chronically treated with ethanol. A solution of ethanol (150 ml/l) was administered as the only drinking fluid for 3 months with a standard solid diet; both food and drink were available ad lib. Lipogenesis in vivo was measured by the incorporation of tritiated water into lipid fractions: non-saponifiable lipid and fatty acids. Non-saponifiable lipid, both in liver and in adipose tissue, was unaffected by ethanol treatment. However, fatty acid synthesis de novo was significantly enhanced in both liver and adipose tissue, by 150 and 300% respectively. Plasma triacylglycerol and non-esterified fatty acid levels were unchanged and plasma glucose concentration slightly increased by ethanol administration. The rate of lipogenesis increased when insulin: glucagon increased twofold due to the effect of ethanol.

Adipose Tissue↗
PubMed1982

[Effect of the administration of nucleotide coenzymes on the lipogenic enzyme changes caused by chronic alcohol intoxication].

Lipogenic enzymes glucose-6-phosphate dehydrogenase, 6-phosphogluconate dehydrogenase, isocitrate dehydrogenase NADP+ soluble and malic enzyme have been determined in the hepatic soluble fraction of rats chronically treated with ethanol and a lipid rich diet. The treatment based on protectives and lipotropic substances administered as nucleotides: UDP-glucose, CDP-choline, S-adenosyl methionine and Coenzyme A, elicits a significant restoration on the activities of G6PDH, 6PGDH and ICDH. These results show that the treatment, on promoting lipid mobilization, could increase the rate of hepatic lipogenesis. The malic enzyme enhanced activities, when ethanol and lipid diet were simultaneously administered, may be interpreted as a requirement for NADPH by the microsomic drug oxidation system.

Alcohol Oxidoreductases↗
PubMed1982

[Topography of the metabolic cycle of 4-aminobutyrate].

This work describes, with some detail the intervention of 4-aminobutyrate as protagonist of a derivation of tricarboxylic cycle. Its vicarial mission is emphasized in connection with its existence in microorganisms (Escherichia coli and Pseudomonas fluorescens), plants (Helianthus tuberosus. Lupinus albus and Agave americana), neoplasic cells (ascitic tumor of Ehrlich and HeLa cells) and animal tissues (adrenal medulla and brain.

Adrenal Medulla↗
PubMed1982

Metabolic repercussion of coenzyme-A (CoA) in experimental ethanol hepatopathy.

The administration of ethanol plus fat diet has been investigated in our laboratory in relation to the experimental fatty liver in rats. Considering that lipid metabolism are markedly altered in these experimental conditions, the present work studies the effect of simultaneous administration of Coenzyme A (CoA) on the alterations produced by ethanol and lipid diet on glycolytic and lipogenic routes. Ethanol was administered in a 15% solution as the only drinking fluid and a high fat diet (45% vegetable fat as total calories) for three months. CoA was intraperitoneally administered at a dose level of 1.0 mg/Kg body weight/day. Enzymatic activities were determined in the soluble fraction of liver homogenates. The methods used for the estimation of the enzymatic activities are described by Bergmeyer. The most significant changes found by the effect of CoA administration correspond to malic enzyme, citrate lyase and 6-phosphogluconate dehydrogenase. Fatty acid synthetase and glycolytic kinases, especially diminished by the effect of fat diet, did not show any significant restoration of their activities when ethanol and CoA were simultaneously administered.

Animals↗
PubMed1982

[Changes caused by thioacetamide in GOT and GPT aminotransferases and glutamate dehydrogenase in rat liver. Ultrastructural study].

Measurements have been made of the hepatic soluble and mitochondrial GOT and GPT and mitochondrial NAD+ glutamate dehydrogenase activities in thioacetamide-treated rats for 30 days. There is a significant fall in the GOT and GPT soluble activities from the effect of chronic thioacetamide administration while the mitochondrial activities become markedly increased in both cases. Glutamate dehydrogenase also increased from the effect of this hepatotoxic substance. Protein determined in the soluble and mitochondrial fractions, showed decreased levels in the cytosolic extracts and increased levels in the mitochondrial ones. Morphological aspects of liver cells showed hypertrophic mitochondria located around the likewise hypertrophic nucleus. The existence of functionally very active mitochondria in the generating liver, induced by thioacetamide, as well as metabolic mechanisms for the regulating control under pathological circumstances, can be a consequence of the increased ammonia concentration.

Acetamides↗
PubMed1982

[Profile of the capacity for lipid synthesis in vivo in various rat tissues: effect of age].

Changes in 3H2O incorporation in vivo to lipid fractions have been studied in rats 1, 3 and 13 months old. The incorporation of tritiated water into non-saponifiable fraction showed and age-dependent decrease in liver. The values were 4.32, 2.91 and 2.56 mumol 3H2O incorporated/g wet weight of liver/hour, at 1, 3 and 13 months respectively. Similar variations could be observed in adipose tissue and in blood. The rates of lower lipogenesis increase markedly from 1 to 3 months (7.02 to 13.36 mumol 3H2O/g/h) and decrease sharply from the 3rd to 13th months (13.36 to 3.75 mumol 3H2O/g/h). The incorporation of radioactivity into blood and adipose tissue fatty acids, also decrease by age.

Adipose Tissue↗
PubMed1982

[Effect of thioacetamide on the incorporation of tritiated water into rat liver phospholipids].

Male Wistar rats received an intraperitoneally daily dose of thioacetamide of 100 mg/kg body weight during 3, 8 and 30 days. Phospholipid levels and radioactive incorporation of 3H2O into total lipids, polar lipids and phospholipids 1 h after intraperitoneal administration of 5 mCi of tritiated water, were determined in livers of untreated control rats and of animal treated during the above mentioned periods. Earlier doses of thioacetamide provoked an increase in the 3H2O incorporation into total lipid fraction. Prolonged treatment resulted in an inhibition of tritiated water incorporation. After three days of thioacetamide administration the incorporated radioactivity in phospholipid fraction decreased. There was also observed a decrease in the radioactivity incorporated into the major phospholipids: phosphatidylcholine and phosphatidyl ethanolamine. However, the levels of these phospholipids showed no significant changes. These observations support the suggestion that de novo biosynthesized fatty acids are being utilized for 1-palmitoyl-2-oleoyl and 1-palmitoyl-2-linoleoyl phospholipids biosinthesis in lesser proportion in rats treated with thioacetamide than in control rats.

Acetamides↗
PubMed1982

[Effect of thioacetamide on the incorporation of 32P into phospholipids of rat liver].

The effect of thioacetamide on rat liver phospholipids biosynthesis was investigated using 32P as precursor. The incorporation of 32P-ortophosphate in the polar lipid fraction and the specific radioactivities of individual phospholipids in the liver fraction and the specific radioactivities of individual phospholipids in the liver of control rats and rats treated with thioacetamide were determined 75 min after intraperitoneal administration of 32P-ortophosphate. Intraperitoneal injection of thioacetamide (daily dose of 100 mg/kg body weight) in male Wistar rats resulted in an increase of 32P incorporation in the over-all phospholipids, after 8 doses administration and a significant decrease during the chronic intoxication. Specific activity of phosphatidylcholine decreased and a parellel increase in specific radioactivity of lisophosphatidylcholine was found after three days of thioacetamide treatment. There was also observed a marked increase in specific radioactivity of sphingomyelin, which could be due to a stimulation of CDP-choline: ceramide cholinephosphotransferase reaction with subsequent diminution of the rate of phosphatidylcholine synthesis via the CDP-amine pathway (involving cytidine diphosphocholine).

Acetamides↗
PubMed1979

The effect of thioacetamide on urea cycle enzymes of rat liver.

The urea cycle enzymes, carbamoyl-P-synthetase, ornithine transcarbamylase, arginase and other enzymes related to ammonia metabolism, such as glutamate dehydrogenase, glutamine synthetase and alanine and aspartate aminotransferases,have been studied in thioacetamide-induced liver disease in rats. Urea and ammonia were determined both in serum and in liver extracts. Glutamate and aspartate were determined in liver extracts. There was a marked decrease (in brackets: fraction of control) in carbamoyl-P-synthetase (0.23), ornithine transcarbamylase (0.36) and arginase (0.62). The accumulation of ammonia (3.22) and the decreased urea level (0.80) are well known indications of liver failure. Glutamate dehydrogenase and glutamine synthetase increased respectively to 1.50 and 1.33, and the changes in glutamate and aspartate levels were respectively 1.68 and 0.92; this indicates that the metabolic route: 2-oxoglutarate leads to glutamate leads to glutamine is increased, and thereby compensates for the low rate of urea formation. Aminotransferase activities were respectively 0.43 and 0.25. No significant differences were found in serum aminotransferases, or in the concentrations of ammonia and urea.

Acetamides↗
PubMed1979

Enzymatic disappearance of hydroxylamine in the presence of GABA.

This paper presents data on the elimination of hydroxylamine from Lupinus albus seeds when they were germinated in the presence of GABA and hydroxylamine. The possibility of an enzymatic reaction. ATP dependent, between GABA and hydroxylamine is discussed. Some kinetic properties from this reaction are studied.

Adenosine Triphosphate↗
PubMed1978

Hepatotoxic effect of thioacetamide (TAM) on NADP-linked enzymes, aminotransferases and glutamate dehydrogenase.

NADP-linked dehydrogenases, glucose-6-P dehydrogenase (G 6PDH) 6-P gluconate dehydrogenase (6 PGDH), isocitrate dehydrogenase (ICDH), malate dehydrogenase decarboxylating (ME) and aminotransferases GOT and GPT were analyzed in the soluble fraction of blood free homogenates. Glutmate dehydrogenase (GDH) was assayed in the mitochondrial fraction. TAM was i.p. administered to male albino rats (50 mg/kg/day) for 28 days. enzyme activities were determined as described by Bermeyer 1965 (Methods Enzymatic Analysis. Verlag Chemie. Acad. Press).

Acetamides↗
PubMed1978

[Studies on the release of dopamine-beta-hydroxylase by nicotine (author's transl)].

Comparative studies were made on the release of DBH by adrenal medullary slices after colinomimetic stimulation with acetylcholine, DMPP or nicotine. The in vivo effects of nicotine on the circulating plasma dopamine-beta-hydroxylase were tested in habitual and non habitual smokers after five cigarettes (12.5 mg of nicotine). The rise of plasma enzyme activity may reflect the increased catecholamine release from adrenal and peripheral adrenergic nerves.

Adrenal Glands↗