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C J Eriksson

Publications and source records attributed to C J Eriksson.

At least 73 records · Page 4Linked to original sources
PubMed1980

Difficulties in measuring human blood acetaldehyde concentrations during ethanol intoxication.

The determination of human blood acetaldehyde (AcH) concentrations is complicated by two artefactual reactions, one resulting in the disappearance of AcH prior to deproteinization of the blood and the other resulting in the formation of AcH during deproteinization. The AcH formation increases with increasing ethanol concentration and decreases with increasing blood dilution, while the rapid AcH disappearance is initiated at the start of the blood collection. The magnitudes of these artefactual reactions are of such an order that a re-evaluation of previous reports on human blood AcH levels is needed. To circumvent these difficulties we suggest that blood should be deproteinized immediately (less than 5s) after arterial or venous puncture and corrections for AcH formation should be determined under the experimental conditions employed. The first data available on human blood AcH concentrations during ethanol intoxication, determined with such methods (20 to 40 micro M AcH after 1 g/kg ethanol), revealed no differences between the estimated in vivo arterial and venous AcH concentrations.

Acetaldehyde↗
PubMed1980

Determination of hepatic acetaldehyde and its biphasic relationship to the ethanol concentration in rats.

In situ freeze clamping of livers using either pentobarbital anaesthesia (40 mg/kg) or cervical dislocation as means of sacrificing rats were compared in regard to the determination of the hepatic acetaldehyde (AcH) concentration following ethanol exposure. It was demonstrated that following cervical dislocation, the AcH concentration decreased by 50%, ethanol decreased by 7%, and the mitochondrial redox state, expressed by the 3-hydroxybutyrate/acetoacetate ratio, increased by 100% within 40 s. The extrapolated 0-time values for AcH, ethanol concentration, and 3-hydroxybutyrate/acetoacetate ratio were equal to values obtained from pentobarbital anaesthetized rats. AcH concentrations (5 to 100 microM) were also measured 60 minutes after administration of increasing doses of ethanol. A positive correlation between the hepatic AcH and ethanol concentration was found up to ethanol concentrations of about 20 mM, suggesting either an increase in ethanol oxidation, a decrease in AcH oxidation, or both were present concomitant with increasing ethanol concentrations. When ethanol concentrations were above 20 mM, a negative correlation between AcH level and ethanol concentration was observed, suggesting a decrease in ethanol oxidation, an increase in AcH oxidation, or both were occurring.

Acetaldehyde↗
PubMed1980

Lack of difference in blood acetaldehyde of alcoholics and controls after ethanol ingestion.

Ethanol and acetaldehyde (AcH) metabolism were studied in male Caucasian alcoholic subjects and matched controls following 1 g/kg ethanol, which was administered after a 10 day, ethanol-free period. The rate of ethanol elimination was higher (p greater than 0.05) in the alcoholics (0.120 g/kg/hr) than in controls (0.108 g/kg/hr). Blood AcH concentrations were measured in either the supernatants of whole blood deproteinized with perchloric acid (PCA) or from the supernatants of PCA-treated plasma obtained from blood added to isotonic semicarbazide. There was no differences between the alcoholic and control subjects for AcH in blood dripped directly into the PCA. The blood AcH concentrations decreased from 22 microM (controls) and 23 microM (alcoholics) to 7 microM (controls) and 3 microM (alcoholics) at 1 and 7 hours after the start of drinking, respectively. No significant AcH was found in blood first taken into heparinized tubes before deproteinization with PCA, after correction for artifactual AcH formation was made. As well, no significant AcH was measured by the semicarbazide method after correction for artifactual AcH. These results suggest that elevated blood AcH levels after ethanol ingestion cannot be taken as a general marker of alcoholism.

Acetaldehyde↗
PubMed1980

Evidence against a biphasic effect of acetaldehyde on voluntary ethanol consumption in rats.

A group of 27 male Long-Evans rats was given a 2 week period of free-choice ethanol and consumed 1.26 +/- 1.27 g/kg/day (mean +/- SD). The animals were then divided into 3 groups. One group received the aldehyde dehydrogenase inhibitor, cyanamide, in their diet and an oral ethanol dose of 2 g/kg for 5 days. Another group received only the oral ethanol dose and the third, control, group received no treatment during these days. After the forced cyanamide and/or forced ethanol treatment, all of the rats were returned to the choice situation. Voluntary ethanol consumption was then followed for 2 months, during which time the control rats steadily increased their ethanol intake to 3.6 +/- 2.1 g/kg/day (mean +/- SD of last week's consumption). The cyanamide treatment caused a transient (3--4 day) decrease in the ethanol intake, after which the consumption increased to 3.7 +/- 2.9 g/kg/day. Consumption by the forced ethanol group (5.4 +/- 2.0 g/kg/day) was significantly greater (p less than 0.05) than that by the other rats. The present results do not favor a physiological role for acetaldehyde-induced formation of alkaloids in increasing voluntary ethanol consumption, but do support the notion of an acetaldehyde-mediated aversive effect on ethanol drinking.

Acetaldehyde↗
PubMed1980

Problems and pitfalls in acetaldehyde determinations.

The determination of acetaldehyde in biologic samples is complicated by a variety of formation and disappearance reactions occurring in the present methods of acetaldehyde analyses. The acetaldehyde formation (ethanol oxidation) in deproteinized supernatant of tissue preparations is prevented by the use of thiourea. During deproteinization, however, it is not inhibited by thiourea, and this remains the main problem in blood acetaldehyde determinations. To circumvent this problem, the use of a correction curve is proposed which is generated by adding control blood samples to the deproteinizing agent such that the blood dilution, temperature, and the ethanol concentrations (the main factors affecting the artifactual acetaldehyde formation) in the controls are identical to those of the samples. Disappearance reactions mainly include loss of acetaldehyde due to binding and/or metabolism. The problem seems to be pronounced with human blood samples, and it is recommended that they be rapidly ( less than 5 sec) deproteinized.

Acetaldehyde↗
PubMed1980

The aversive effect of acetaldehyde on alcohol drinking behavior in the rat.

There are a number of indications suggesting that acetaldehyde (AcH) is one factor affecting the alcohol drinking behavior in laboratory animals. In the present study, the voluntary alcohol consumption in a free-choice situation was recorded in 17 females Sprague-Dawley rats fed with two different diets. The first diet (commercial Astra-Ewos, Sweden) caused significantly (p less than 0.001) higher blood AcH concentrations after oral alcohol administration and lower alcohol preferences (alcohol intake as percentage of total fluid intake) than the other diet (prepared at the Alko laboratories). With the Alko diet, the individual preference values correlated negatively with the blood AcH concentrations (p less than 0.01) and positively with the liver aldehyde dehydrogenase activities (p less than 0.05). Hepatic alcohol oxidation rate was found to correlate positively with the AcH concentrations from perfused livers (p less than 0.05) and negatively with the alcohol preferences (p less than 0.05), Alko diet). The results are discussed considering a possible biphasic relation between the AcH metabolism and alcohol drinking behavior.

Acetaldehyde↗
PubMed1977

Regulation of acetaldehyde metabolism during ethanol oxidation in perfused rat liver.

Acetaldehyde (AcH) metabolism during ethanol oxidation has been studied in once-through perfused rat livers. The interest was focused upon the interrelations between the hepatic AcH concentration, AcH oxidation rate, ethanol metabolism, cytosolic and mitochondrial redox state, and aldehyde dehydrogenase (ALDH) activity. Correlational analyses between the possible regulative factors and regulated parameters were made and the following main conclusions drawn. The AcH concentration leaving the liver during the ethanol metabolism was regulated by both the ethanol and AcH oxidation rates, which in turn were regulated by the cytosolic redox state and the ALDH activity, respectively.

Acetaldehyde↗
PubMed1977

Acetaldehyde metabolism in vivo during ethanol oxidation.

The liver is the primary site for the oxidation of ethanol-derived acetaldehyde (AcH) in the rat. Only a small amount of the total AcH formed in this organ escapes into the rest of the body, but this amount increases with increasing hepatic ethanol concentrations. The bulk of the hepatic AcH output is eliminated extrahepatically, thus drastically changing the AcH level from that initially leaving the liver. Nevertheless, the extrahepatic blood AcH levels can be used as relatively accurate indicators of the corresponding hepatic AcH levels, since they are highly correlated with them. Significant levels of brain AcH occur only at very high arterial blood AcH concentrations.

Acetaldehyde↗
PubMed1976

Effects of fructose and glucose on ethanol-induced metabolic changes and on the intensity of alcohol intoxication and hangover.

The effects of fructose and glucose on the metabolic changes induced by ethanol and on the intensity of alcohol intoxication and hangover were studied in 109 healthy male volunteers. After 10 hours of fasting, the subjects were given 1.75 g of ethanol per kg body wt during 3 hours under controlled laboratory conditions. Fructose or glucose were adminstered either simultaneously with ethanol or 12 hours later during the hangover period. The intensity of alcohol intoxication and hangover were estimated 10 times during the experimental period of 20 hours using subjective and objective rating scales. Sequential determinations of blood ethanol, acetaldehyde, glucose, lactate, free fatty acids, triglycerides, ketone bodies and capillary blood acid-base balance were also made during the experiment. Under these experimental conditions neither fructose nor glucose had any significant effect on the intensity of alcohol intoxication and hangover. The sugars also had no significant effect on the rate of ethanol elimination or on the blood acetaldehyde concentration during the course of the experiment. Blood glucose concentration was decreased and blood lactate, free fatty acid and ketone body concentrations were increased during the hangover period in the subjects who had been given only ethanol. These subjects also had a marked metabolic acidosis during hangover. Glucose and fructose significantly inhibited the metabolic alterations induced by ethanol. In this respect fructose was more effective than glucose. The results indicate that both fructose and glucose effectively inhibit the metabolic disturbances induced by ethanol but they do not affect the symptoms or signs of alcohol intoxication and hangover. The results support the view that hangover is not directly related to the metabolic effects of ethanol or to its metabolic products.

Acetaldehyde↗