[Change in the functional state of the adrenal cortex due to alcoholic intoxication].
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An acute intraperitoneal administration of ethanol (4-8 g/kg) produced a fall in the activity of malate-dehydrogenase (MDG), alanine- and aspartate-aminotransferase in homogenates and mitochondria of the cerebellum, large hemispheres and liver of the rats by 25 and 50 per cent, respectively. The activity of succinate-dehydrogenase (SDG) increased by 24 per cent in the large hemispheres and fell by 20 per cent in the liver and in the cerebellum homogenate. The activity of lactate-dehydrogenase (LDG) of the large hemispheres and liver mitochondria decreased by 30 per cent. A chronic (1 1/2-2 month long) ethanol intoxication produced a drop of the LDG and MDG in the mitochondria of the nerve structures and of aminotransferase in the liver. The SDG activity rose in the homogenate of the cerebellum, large hemispheres and of the liver by 80, 50 and 20 percent, respectively. The dehydrogenases and aminotransferases activity in the liver and nerve structures of rats in the state of abstinence was somewhat below the normal, but higher than in animals chronically consuming alcohol.
Authors report on the analysis of long-term effectiveness of rehabilitation programs for multiple drinking-driving offenders. Even after an observation-period of 60 months since license renewal after treatment, program participants show a lower reconviction-rate than drivers who had been judged qualified to drive after medical and psychological assessment. Hence, there is no evidence for a mere deceleration of recidivism but on the contrary for long-term effectiveness. The analysis comprised the influence of individual variables such as age, previous DWI offenses, BAC in the event of DWI, previous criminal offenses, medical symptoms of alcohol-dependence and on the other hand systematic effects such as intensity of law enforcement by the police and regional drinking-habits. Furthermore the effects of three different treatment programs on the long-term reconviction rate are analysed and presented. The study discusses a number of critical arguments with respect to methodology and recommends consequences for future assessment and treatment. On the background of the problems of an extended observation period in the field--changes of variables of influence on drinking and drinking-driving behavior are possible, which cannot be compensated by treatment--the results are judged highly satisfying. They do not only justify continuing treatment after assessment but lead to the recommendation to extend treatment.
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A single intraperitoneal administration of ethanol (3.5 g/kg) to rats induced a marked increase in lipid peroxidation and a decrease of antioxidative activity in the liver after 1 h when assessed by chemi-luminescence in liver homogenates. The pretreatment with aldehyde dehydrogenase inhibitor, disulfiram (200 mg/kg 24 hr before ethanol), caused a 10-fold elevation of the blood acetaldehyde levels, with no effect on the hepatic lipid peroxidation compared to control. Cyanamide (50 mg/kg, 2 h before the ethanol) increased approximately 100-fold the acetaldehyde levels, however, the changes in lipid peroxidation were not significantly different from that produced by ethanol alone. The present results suggest, that the metabolism of acetaldehyde and not acetaldehyde itself is responsible for the in vivo activation of lipid peroxidation during acute alcohol intoxication. Disulfiram prevents the ethanol-induced lipid peroxidation in the rat liver.
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