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Biomedical subjects

A J Barak

Publications and source records attributed to A J Barak.

At least 37 records · Page 2Linked to original sources
PubMed1979

A simplified procedure for the determination of betaine in liver.

A convenient procedure for the determination of hepatic betaine levels is described. The method takes advantage of ethanol precipitation to rid acidified tissue extracts of interfering substances. Betaine is reacted with potassium triiodide to form betaine periodide, which is selectively precipitated via pH adjustment. The precipitate of betaine periodide is dissolved in ethylene dichloride and measured spectrophotometrically. The method is specific, accurate, and simple and showed recoveries of from 97 to 103% at two different levels of added betaine. The applicability of the method was shown when it was demonstrated that diets containing different amounts of choline influenced levels of hepatic betaine.

Animals↗
PubMed1979

Determination of the site of zinc absorption in rat small intestine.

We have studied net uptake of zinc from segments of rat duodenum, jejunum, and ileum using in vivo intestinal perfusion. We have also evaluated the effect of pancreatic and bile secretions on duodenal zinc absorption. Segments of duodenum, jejunum, and ileum and duodenum with bile and pancreatic duct obstruction, 10 cm in length, were studied in six rats each. Percentage absorption of zinc as determined by atomic absorption spectrophotomety was greater from the ileum (60.1%) when compared to duodenum (19.1%) or jejunum (20.2%). Exclusion of bile and pancreatic secretions from the lumen increased zinc absorption in the duodenum (32.0%). Postperfusion mucosal zinc content comprised 29.0% of absorbed zinc from jejunum, 7.4% from ileum, 5.2% from duodenum, and 2.7% from duodenum with bile and pancreatic duct obstructed, indicating rapid transport of zinc across epithelial cells after uptake from the duodenum and ileum. Our data indicate that the ileum has the greatest capacity for zinc absorption.

Animals↗
PubMed1979

Malignant hyperthermia. A potentially fatal syndrome in orthopaedic patients.

Malignant hyperthermia is an inherited muscular disorder and a cause of sudden death in afflicted patients. Stress arising from tramuma, surgery, and other causes can initiate the syndrome. We studied the types of orthopaedic problems commonly seen in patients with this condition as well as the clinical manifestations and pathophysiology of the syndrome. Recognition, management, and understanding of the pathophysiology of malignant hyperthermia can be aided by a study of its similarities to porcine stress syndrome. We performed experimental studies of muscle and prophylaxis in swine. We also demonstrated the extension of the prophylactic use of dantrolene sodium in a management protocol in eighty surgical procedures in humans.

Adult↗
PubMed1978

Assay for free and total choline activity in biological fluids and tissues of rats and man with Torulopsis pintolopessi.

The sensitive, specific growth response to choline activity of the thermophilic enteric yeast Torulopsis pintolopessi enables estimation of free and bound choline activity in rat and human fluids and tissues- as little as 10 ng/ml of choline is measurable. Unlike other microbial assays, estimation of unbound (free) choline activity is not influenced by methionine or phospholipids. The method also distinguishes differences in choline activity of fluids and tissues from choline-deficient and choline-replete rats. Free and bound choline activity in blood, red blood cells, plasma, and liver from choline-deficient rats were almost 2-fold lower than from choline-supplemented animals. Free and bound choline activity in whole brain from choline-deficient rats were signifigantly higher (more than 2-fold). The application of the T. pintolopessi method in studying choline status in man and reasons for high choline activity in brain of choline-deficient rats are suggested.

Adult↗
PubMed1978

Effects of phenobarbital administration on levels of physiological antioxidants in rat liver.

Administration of phenobarbital to rats over a period of 5 days was shown to increase hepatic lipid peroxidation concomitant with induction of cytochrome P-450 and cytochrome c reductase. The purpose of this study was to determine whether the increase in lipid peroxidation was due to a lowering in hepatic antioxidants. The results show that increased lipid peroxidation was not due to a decreased level of antioxidants since the fat-soluble antioxidants were unchanged and ascorbate, a water-soluble antioxidant, was elevated. The relationship of the increase in hepatic ascorbate to enhanced lipid peroxidation is discussed.

Animals↗
PubMed1977

Role of acetaldehyde in the ethanol-induced impairment of glycoprotein metabolism in rat liver slices.

The mechanism responsible for ethanol-induced changes in the glycosylation of proteins was investigated in rat liver slices. Ethanol (5 to 50 mM) decreased [1-14C]glucosamine and [14C]leucine incorporation into total liver and microsomal proteins and greatly inhibited incorporation into medium (secretory) proteins. Pyrazole prevented the inhibition of glycoprotein synthesis by ethanol. Additions of methylene blue or pyruvate, which corrected the disordered redox state caused by ethanol oxidation, did not reverse the inhibitory effects of ethanol on glycosylation. Sorbitol, which mimics ethanol in generating reducing equivalents in the hepatocyte, also inhibited glycosylation; however, fructose, the immediate oxidation product of sorbitol, similarly inhibited glycoprotein synthesis without altering the redox state. When low levels of acetaldehyde (0.12 to 0.70 mM) were maintained in the medium by means of infusion, a significant inhibition of glycoprotein synthesis was observed. Acetate did not impair glycosylation. These data suggest that the ethanol-induced impairment of glycoprotein synthesis and secretion is a consequence of ethanol metabolism and further suggest that this inhibition is attributable to acetaldehyde formation rather than to the altered redox state resulting from ethanol oxidation.

Acetaldehyde↗
PubMed1977

Evidence that acetaldehyde irreversibly impairs glycoprotein metabolism in liver slices.

When liver slices were incubated for 1 hr in a medium containing either acetaldehyde or ethanol and then switched to a fresh medium free from acetaldehyde but containing the appropriate radioactive precursors and reincubated for 3 additional hr, a decreased incorporation of both [14C]glucosamine and [14C]leucine into hepatocellular and secretory proteins was observed. Further studies were carried out comparing the inhibitory effects of ethanol and acetaldehyde on drug metabolism. Higher concentrations of ethanol were necessary to impair aniline hydroxylation when compared to its effect on glycoprotein metabolism. Acetaldehyde did not affect aniline metabolism, suggesting some specificity for its effect on intracellular metabolic functions. Our results show that the acetaldehyde-induced inhibition of glycoprotein synthesis is irreversible under these short term experimental conditions and is not dependent on the physical presence of acetaldehyde in the incubation medium.

Acetaldehyde↗
PubMed1976

Potentiation of ethanol fatty liver in rats by chronic administration of nicotinic acid.

Two groups of rats were fed isocalorically on alcohol and control semi-liquid diet for 28 days; two other groups had the same diets except for supplementation with nicotinic acid at 50 mg/100 ml of diet, Blood ethanol levels were unaffected by nicotinic acid administration, even though nicotinic acid was well absorbed and stored in the liver. Lipid analyses of liver and plasma after 28 days revealed that nicotinic acid, per se, stimulated fatty infiltration of the liver and this effect was potentiated when given in conjunction with ethanol.

Animals↗
PubMed1976

Paradoxical urinary excretion of D-glucaric acid in acute viral hepatitis.

The urinary excretion of D-glucaric acid and the plasma clearance of antipyrine were estimated during the acute phase of viral hepatitis and again during recovery. The plasma clearance of antipyrine was impaired during the acute stage of hepatitis, while the urinary excretion of D-glucaric acid was paradoxically high. Both parameters returned to normal during recovery. These findings suggest that the use of urinary D-glucaric acid excretion as an index of microsomal enzyme induction is unreliable when there is liver injury.

Acute Disease↗
PubMed1976

Altered elimination of antipyrine in patients with acute viral hepatitis.

The plasma half-life and clearance of antipyrine was investigated in patients during the acute phase and again during the recovery phase of viral hepatitis. Each patient served as his own control, thereby eliminating genetic factors and minimising environmental factors that cause large interindividual variations in antipyrine elimination rates. Liver function tests, antipyrine, half-life, plasma clearance, and the apparent volume of distribution were determined in the acute and recovery period. It was found that the appaarent volume of distribution of antipyrine did not change in five of six patients as they recovered. Five of the six patients showed prolonged plasma half-lives and decreased plasma clearance of the drug at the time of acute illness and these parameters reached normal values during recovery. The plasma half-life and clearance of the drug did not correlate with biochemical indices of liver function in the recovery phase. This demonstration supports the concept that drug metabolism is frequently impaired in liver disease.

Adult↗
PubMed1975

Inability of selenium to affect creatine metabolism in rat muscle.

1. Two groups of adult rats were placed in a metal-free environment and pair-fed with selenium-supplemented and Se-deficient diets. 2. After 5 months the animals were killed and skeletal muscle concentrations of creatine, creating phosphate, ATP, protein and Se were determined. 3. Se deficiency was indicated by the low Se content of the skeletal muscle from the deficient animals, but no changes were found in the amounts of the other components. 4. These results suggest that Se may not be involved in creatine metabolism and that Se deficiency may not be concerned independently in the development of nutritional dystrophy, where changes are found in the levels of protein, creatine, creatine phosphate and ATP.

Adenosine Triphosphate↗