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Biomedical subjects

M Rusi

Publications and source records attributed to M Rusi.

6 recordsLinked to original sources
PubMed1981

Brain aldehyde dehydrogenase activity in rat strains with high and low ethanol preferences.

The activity of aldehyde dehydrogenase in subcellular fractions of whole brain homogenates from the AA and ANA rat strains developed respectively for high and low ethanol preferences has been studied. No significant strain or sex differences between naive AA and ANA rats were found. In ethanol-experienced rats some strain and sex differences were found, the most consistent being higher enzyme activity in AA females than in males both with aliphatic and aromatic aldehyde substrates. However, contrary to previous findings no relation between brain aldehyde dehydrogenase activity and drinking behavior was found in the AA and ANA rat strains.

Aldehyde Dehydrogenase↗
PubMed1980

Renin, water drinking, walt preference and blood pressure in alcohol preferring and alcohol avoiding rats.

Mechanisms controlling fluid volume were studied in alcohol preferring AA (Alko, Alcohol) and alcohol avoiding ANA (Alko, Non-Alcohol) rats. Hypertonic sodium chloride solution (5%) given orally caused a higher dipsogenic response in AA rats than in the ANA's. One hour after ethanol loading (4.8 g/kg, by stomach tube), plasma renin activity of AA rats was four times as high as in ANA rats. ANA rats had higher degree of sodium chloride (0.9%) preference and higher blood pressure. The strain differences in voluntary salt intake and salt metabolism may modulate the consumption of calories and water as well as blood pressure and different reactivity of the renin system in AA and ANA rats.

Alcohol Drinking↗
PubMed1980

The effects of dietary thiamin on voluntary ethanol drinking and ethanol metabolism in the rat.

1. The influence of a deficiency or surplus of thiamin in the diet on voluntary ethanol consumption, ethanol elimination rate and blood acetaldehyde concentration was studied in rats. 2. Both the high-thiamin diet containing 20 mg thiamin hydrochloride/kg and the thiamin deficient diet containing no measurable thiamin produced obvious functional effects on thiamin metabolism in rat tissues after 4 weeks as demonstrated by measurements of the blood transketolase (sedoheptulose-7-phosphate: D-glyceraldehyde-3-phosphate glycolaldehyde-transferase; EC 2.2.1.1) activity and the extent of thiamin pyrophosphate-stimulation of the enzyme. 3. During the first week on the test diets the prospective ethanol free-choice groups had 1.72 M-ethanol as their only drinking-fluid. Subsequently they had a choice between ethanol and tap water for three weeks. During the free-choice period the rats on the high-thiamin diet drank only one-fifth as much ethanol as the rats given the optimum diet with 4 mg thiamin hydrochloride/kg. 4. The thiamin-deficient rats showed a significant tendency to increase ethanol drinking, when intake was expressed relative to total energy intake, but their intake of ethanol on a g/kg body-weight basis was approximately the same as that of the group given the optimum-diet. 5. The observed differences in voluntary ethanol drinking associated with different levels of dietary thiamin cannot be explained by changes in the ethanol elimination rate or the acetaldehyde accumulation in blood during the oxidation of ethanol.

Acetaldehyde↗
PubMed1979

The effects of dietary niacin and riboflavin on voluntary intake and metabolism of ethanol in rats.

The effects of dietary deficiency and excess of niacin and riboflavin on voluntary drinking of 10% (v/v) ethanol were studied in male rats. The effectiveness of dietary deficiency and excess of both niacin and riboflavin on tissue levels of these vitamins was demonstrated by measurements of urinary N1-methylnicotinamide and blood glutathione reductase (EC 1.6.4.2) activity. A high-niacin diet containing 75 mg niacin/kg food decreased ethanol intake by about 36% compared to the control diet containing 15 mgniacin/kg. Niacin or riboflavin deficiency and a high-riboflavin diet containing 40 mg rtary levels of niacin or riboflavin did not influence on ethanol elimination rate or levels of blood acetaldehyde during ethanol oxidation. Therefore, blood acetaldehyde was not responsible for the decreased ethanol intake of rats fed with a high-niacin diet. It was concluded that the increased ethanol intake caused by dietary deprivation of B-vitamin complex found in earlier studies is not a result of deficiency of niacin or riboflavin but niacin may be involved in the decrease in ethanol drinking, which follows dietary B-vitamin complex supplementation.

Acetaldehyde↗