ABSTRACT
Red cell aldehyde dehydrogenase (ALDH, EC 1.2.1.3) activity was measured by spectrophotometry in normal subjects and alcoholics after various periods of alcohol abstinence. ALDH was measured in all red cell hemolysate fractions; red cells were purified from hemoglobin by Sephadex CM-50 chromatography. The enzyme activity was found reduced in alcoholics' red cells as against that in controls. ALDH activities were somewhat increasing and approaching the normal values in the patients not using ethanol for 4 weeks or longer. These results recommend ALDH measurements in human red cells as a test for the detection of subjects abusing alcohol.
Subject(s)
Alcoholism/enzymology , Aldehyde Dehydrogenase/blood , Erythrocytes/enzymology , Adult , Alcoholism/blood , Humans , Male , Middle AgedABSTRACT
White rats were divided into water-preferring (WP) and ethanol-preferring (EP) groups, on the basis of their preferable drink: either water or 15% solution of ethanol. Each of these groups was then subdivided into groups which were given to drink for 1 year 15% solution of ethanol (ethanol-treated) or water (controls). Alcohol dehydrogenase/aldehyde dehydrogenase activity ratios (ADH/AlDH) in livers of WP controls were considerably higher than those in EP controls. The difference in ADH/AlDH has somewhat decreased after ethanol treatment. However, this ratio remained the highest in the WP alcohol-treated group. The signs of proteinic and lipid dystrophy of the liver in alcohol-treated WP rats were expressed much more clearly than in all other groups. It is concluded that in the liver of animals with a high ADH/AlDH ratio there are favourable conditions for accumulation of a toxic hepatocyte-damaging acetaldehyde.
Subject(s)
Alcohol Dehydrogenase/metabolism , Aldehyde Dehydrogenase/metabolism , Ethanol/toxicity , Liver/drug effects , Alcoholism/enzymology , Alcoholism/etiology , Alcoholism/pathology , Animals , Liver/enzymology , Liver/pathology , Male , Rats , Time FactorsABSTRACT
Alcohol dehydrogenase activity (ADH; KP 1.1.1.1.) in blood serum of rats and rabbits is 1 and 2 orders of magnitude higher than in humans. In chronic alcoholics, blood ADN is activated with an increase in alcoholism standing. Twelve hours after acute alcoholic intoxication alcoholics and heavy drinkers manifest a significant reduction in blood ADH activity. Acute alcoholic intoxication does not influence blood ADH in men who do not abuse alcohol. Chronic exposure of rabbits to ethanol leads to a decrease in ADH activity in the liver and to its rise in the blood. ADH activation is observed only in those animals which demonstrate the signs of fatty and protein liver dystrophy. It is concluded that chronic exposure to ethanol does not induce ADH synthesis in the liver. The blood ADH content ascends as a results of an increase in ADH transport from hepatocytes to the bloodstream.
Subject(s)
Alcohol Oxidoreductases/blood , Alcoholic Intoxication/enzymology , Alcoholism/enzymology , Adult , Animals , Dose-Response Relationship, Drug , Drug Tolerance , Humans , Liver/enzymology , Male , Middle Aged , Rabbits , Rats , Rats, Inbred Strains , Time FactorsABSTRACT
A study was made of the RNA biosynthesis intensity in the brain cortex depending on the rate of the learning of the conditioned active avoidance and food reinforcement alteration responses in ethanol or water preferring rats placed in a complex maze. The level of the brain RNA biosynthesis in ethanol preferring rats was lower as compared with that in rats preferring water. In ethanol preferring rats, the rate of the learning of the conditioned active avoidance response was lower, whereas that of the learning of the alternation response was greater than in water preferring rats. The data are discussed in accordance with the concepts that disorders in the interaction of transmitter and genetic structures of brain cells form the basis of the behavior of ethanol preferring animals.
Subject(s)
Alcohol Drinking , Behavior, Animal/drug effects , Drinking Behavior/physiology , Animals , Avoidance Learning/drug effects , Cell Nucleus/drug effects , Cell Nucleus/metabolism , Cerebral Cortex/drug effects , Cerebral Cortex/metabolism , Conditioning, Classical/drug effects , Male , RNA/biosynthesis , RatsABSTRACT
Cross immunoelectrophoresis was used to study antigenic composition of the brain of rats preferring water, or 15% ethanol and of intermediate group animals. The rat brain showed 6 antigens, one of them was found to be neurospecific. The intermediate group animals and those preferring ethanol differed from those preferring water in that they demonstrated two antigens which were found to be neuro-nonspecific. The content of the neurospecific protein S-100 in the cerebellum measured by rocket immunoelectrophoresis was demonstrated to be the same in animals preferring water and ethanol. A single intraperitoneal injection of 25% ethanol (2.5 g/kg) to the intermediate group rats brought about a change in the composition of neuro-nonspecific soluble antigens of the brain.
Subject(s)
Alcoholic Intoxication/immunology , Antigens/analysis , Brain/immunology , Nerve Tissue Proteins/immunology , Animals , Humans , Immunoelectrophoresis, Two-Dimensional , Male , RatsABSTRACT
Content of lipids and apolipoproteins A-1 and E was studied in blood plasma of men with acute alcohol intoxication as well as within 10-12 hrs after their treatment in a special clinic. Acute alcohol intoxication caused a distinct increase of triglycerides as well as of cholesterol in high and very low density lipoproteins simultaneously with decrease in content of cholesterol in low density lipoproteins. At the same time, content of apolipoprotein A-1 was increased and of apo E--unaltered. Within 12 hrs after treatment of the men concentrations of triglycerides and cholesterol of very low density lipoproteins became quite normal but the other patterns studied did not alter. Alcohol appears to affect the distribution of cholesterol between individual lipoprotein fractions in blood. This process depended distinctly on alteration of apo A-1 concentration in blood plasma.
