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Biomedical subjects

J Bernstein

Publications and source records attributed to J Bernstein.

At least 307 records · Page 17Linked to original sources
PubMed1975

Effects of chronic ethanol treatment and thyroxine administration on ethanol metabolism and liver oxidative capacity.

Chronic administration of ethanol to rats leads to an increase in the rate of ethanol metabolism in vivo and in vitro. In vitro studies in liver slices showed that ouabain, an inhibitor of the Na++K+-activated adenosine triphosphatase, can completely block the extra ethanol metabolism in the livers of the treated animals only in the presence of ouabain. Administration of thyroxine led to an increase in the rate of ethanol metabolism when measured both in vitro and in vivo. This effect was biphasic; an activation occurred only with low doses of thyroxine but disappeared after administration of larger doses. Alcohol dehydrogenase activity in the liver of the animals treated with large doses of thyroxine was found to be significantly reduced. With the doses used (50-1000 mug/kg), thyroxine also increased the rate of oxygen consumption as measured in liver slices. However, a biphasic effect did not occur; a near maximum activation on the rate of oxygen consumption occurred with low doses of thyroxine (100 mug/kg). Oxygen consumption was also found to be increased in the liver of animals chronically treated with ethanol. A maximal effect was produced after 18 to 21 days of treatment. For both ethanol and thyroxine-treated animals, an increased rate of oxygen consumption occurred with a concomitant loss of dinitrophenol effect. Mitochondrial alpha-glycerophosphate oxidase was found to be increased in the liver of animals treated with ethanol or with thyroxine. In these two groups, this enzymatic activity appeared to be less affected by the treatment than the dinitrophenol-activated respiration.

Alcohol Oxidoreductases↗
PubMed1975

Hormonal influences in the development of the hypermetabolic state of the liver produced by chronic administration of ethanol.

Chronic administration of ethanol to rats, either in liquid diets as the only source of food or by gastric intubation while the animals are fed ad libitum, leads to the development of a hypermetabolic state of the liver. This hypermetabolic condition of the liver can be observed independently of the feeding state of the animals. The calorigenic effects produced by ethanol in the liver, as measured in liver slices, could be reproduced by a single large dose of epinephrine. Oxygen consumption by liver slices of animals given a 2-mg/kg dose of epinephrine bitartrate increased by 40 to 50 percent. In these livers all the extra oxygen consumption, but not the basal respiration, could be abolished by ouabain, an inhibitor of the sodium pump. Dinitrophenol did not affect the respiratory rate in the liver of epinephrine-treated animals while markedly increasing that in controls. In the liver of treated animals, the activatory effect of dinitrophenol could be recovered in the presence of ouabain. The calorigenic effect of epinephrine in the liver was found to be completely abolished by phentolamine (alpha adrenergic blocker) but was not modified by DL-propranolol (beta adrenergic blocker). Also, the calorigenic effects produced by epinephrine could not be seen in thyroidectomized animals or by incubating the liver slices in a calcium-free medium. Thyroidectomy and administration of phentolamine markedly reduced and adrenalectomy completely abolished the hypermetabolic state produced in the liver of rats by chronic administration of ethanol.

Adrenal Glands↗
PubMed1974

The renal lesion in syndromes of multiple congenital malformations. Cerebrohepatorenal syndrome; Jeune asphyxiating thoracic dystrophy; tuberous sclerosis; Meckel syndrome.

Renal malformations in cerebrohepatorenal and the Jeune syndromes are variable, encompassing both focal cystic change and severe cystic dysplasia. Morphologic differences might reflect either genetic heterogeneity or injury to the kidney by an underlying metabolic defect at differing times in renal development. The renal lesion in the Meckel syndrome is cystic dysplasia with markedly defective nephronic differentiation. A histologically distinctive cystic tubular lesion is identified in tuberous sclerosis. These lesions must be differentiated from infantile and adult polycystic disease.

Abnormalities, Multiple↗
PubMed1973

Metabolic alterations produced in the liver by chronic ethanol administration. Increased oxidative capacity.

1. Administration of ethanol (14g/day per kg) for 21-26 days to rats increases the ability of the animals to metabolize ethanol, without concomitant changes in the activities of liver alcohol dehydrogenase or catalase. 2. Liver slices from rats chronically treated with ethanol showed a significant increase (40-60%) in the rate of O(2) consumption over that of slices from control animals. The effect of uncoupling agents such as dinitrophenol and arsenate was completely lost after chronic treatment with ethanol. 3. Isolated mitochondria prepared from animals chronically treated with ethanol showed no changes in state 3 or state 4 respiration, ADP/O ratio, respiratory control ratio or in the dinitrophenol effect when succinate was used as substrate. With beta-hydroxybutyrate as substrate a small but statistically significant decrease was found in the ADP/O ratio but not in the other parameters or in the dinitrophenol effect. Further, no changes in mitochondrial Mg(2+)-activated adenosine triphosphatase, dinitrophenol-activated adenosine triphosphatase or in the dinitrophenol-activated adenosine triphosphatase/Mg(2+)-activated adenosine triphosphatase ratio were found as a result of the chronic ethanol treatment. 4. Liver microsomal NADPH oxidase activity, a H(2)O(2)-producing system, was increased by 80-100% by chronic ethanol treatment. Oxidation of formate to CO(2)in vivo was also increased in these animals. The increase in formate metabolism could theoretically be accounted for by an increased production of H(2)O(2) by the NADPH oxidase system plus formate peroxidation by catalase. However, an increased production of H(2)O(2) and oxidation of ethanol by the catalase system could not account for more than 10-20% of the increased ethanol metabolism in the animals chronically treated with ethanol. 5. Results presented indicate that chronic ethanol ingestion results in a faster mitochondrial O(2) consumption in situ suggesting a faster NADH reoxidation. Although only a minor change in mitochondrial coupling was observed with isolated mitochondria, the possibility of an uncoupling in the intact cell cannot be completely discarded. Regardless of the mechanism, these changes could lead to an increased metabolism of ethanol and of other endogenous substrates.

Journal Article↗
PubMed1973

Metabolic alterations produced in the liver by chronic ethanol administration. Changes related to energetic parameters of the cell.

1. Chronic ethanol administration to rats for 21-27 days increases the rate of O(2) consumption as measured in liver slices. The extra respiration can be abolished by inhibition of the active transport of Na(+) and K(+). Dinitrophenol activates the respiratory rate in the liver of the treated animals only in the presence of ouabain. 2. Active (ouabain-sensitive) transport of (86)Rb and (Na(+)+K(+))-stimulated adenosine triphosphatase activity were increased in the livers of the ethanol-treated animals. 3. Chronic ethanol administration also led to a decrease in the phosphorylation potential ([ATP]/[ADP][P(i)]) in the liver cell owing to a decrease in [ATP] and an increase in [P(i)]. 4. It is suggested that an increased sodium pump activity is responsible for the increased oxidative capacity and for the insensitivity to dinitrophenol observed in the livers of ethanol-treated animals.

Journal Article↗
PubMed1973

Metabolic alterations produced in the liver by chronic ethanol administration. Comparison between the effects produced by ethanol and by thyroid hormones.

1. Liver slices from rats treated with thyroxine show an increased rate of O(2) consumption. The extra consumption, but not the basal respiration, can be abolished by ouabain. 2. Dinitrophenol is not effective in increasing the rate of O(2) consumption of liver slices from thyroxine-treated animals but its effectiveness can be recovered in the presence of ouabain. 3. (Na(+)+K(+))-stimulated adenosine triphosphatase activity of liver was increased by administration of thyroxine in vivo. No changes were found in total Mg(2+)-stimulated adenosine triphosphatase activity. 4. Mitochondrial alpha-glycerophosphate dehydrogenase and microsomal NADPH oxidase activity were increased by both thyroxine and chronic ethanol treatment. 5. Liver slices from animals chronically treated with ethanol synthesize urea at an increased rate. 6. Mitochondrial size (section area) is markedly increased in the liver of animals chronically treated with ethanol. 7. Acute administration of ethanol in doses of 4 and 6g/kg significantly increases the uptake of (131)I-labelled thyroxine by the liver. 8. Work reported here, along with results from other investigators, indicates marked similarities between the effects produced in the liver by chronic administration of ethanol and by thyroid hormones.

Journal Article↗