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Biomedical subjects

A Helander

Publications and source records attributed to A Helander.

94 records · Page 6Linked to original sources
PubMedDate not supplied

Biochemical markers of alcohol use and abuse: experiences from the Pilot Study of the WHO/ISBRA Collaborative Project on state and trait markers of alcohol. International Society for Biomedical Research on Alcoholism.

The development of reliable diagnostic tools for assessing alcoholism and harmful alcohol consumption is an utmost necessity for the success of efforts to prevent and treat alcohol-induced damage to both individuals and to society. A multinational study is underway to aid in the development of biological screening tools (state markers) which can, with good sensitivity and specificity, identify problem drinkers. To attain this goal information needs to be available on an individuals's drinking history and habits and related factors. A detailed instrument has been developed to obtain this information. The second goal of the study was to begin to develop diagnostic 'trait markers' which provide biological information on genetically determined predisposing and protective factors in the development of alcoholism. The developed questionnaire also provides background information on subject characteristics necessary for the development of trait markers. Centres will assay the obtained biological samples for 'traditional' and newly identified state markers of excessive alcohol consumption. These will include methanol measurements, gamma-glutamyltransferase, aspartate aminotransferase, carbohydrate-deficient transferrin, serotonin metabolite ratios, and erythrocyte aldehyde dehydrogenase. DNA obtained from the lymphocytes of subjects will be assayed for polymorphisms of alcohol- and aldehyde-metabolizing enzymes and dopamine receptor polymorphisms which can provide insights into protective and predisposing factors in alcoholism. The platelet enzymes, monoamine oxidase and adenylyl cyclase, will be assayed to assess the relationships between these putative trait markers and the genetic and environmental factors contributing to the aetiology of alcoholism. The current report is meant to introduce the study design and present a portion of the preliminary data gathered in the process of establishing this research programme.

Adolescent↗
PubMedDate not supplied

Urinary excretion of methanol and 5-hydroxytryptophol as biochemical markers of recent drinking in the hangover state.

Twenty healthy social drinkers (9 women and 11 men) drank either 50 g of ethanol (mean intake 0.75 g/kg) or 80 g (mean 1.07 g/kg) according to choice as white wine or export beer in the evening over 2 h with a meal. After the end of drinking, at bedtime, in the following morning after waking-up, and on two further occasions during the morning and early afternoon, breath-alcohol tests were performed and samples of urine were collected for analysis of ethanol and methanol and the 5-hydroxytryptophol (5-HTOL) to 5-hydroxyindol-3-ylacetic acid (5-HIAA) ratio. The participants were also asked to quantify the intensity of hangover symptoms (headache, nausea, anxiety, drowsiness, fatigue, muscle aches, vertigo) on a scale from 0 (no symptoms) to 5 (severe symptoms). The first morning urine void collected 6-11 h after bedtime as a rule contained measurable amounts of ethanol, being 0.09 +/- 0.03 g/l (mean +/- SD) after 50 g and 0.38 +/- 0.1 g/l after 80 g ethanol. The corresponding breath-alcohol concentrations were zero, except for three individuals who registered 0.01-0.09g/l. Ethanol was not measurable in urine samples collected later in the morning and early afternoon. The peak urinary methanol occurred in the first morning void, when the mean concentration after 80 g ethanol was approximately 6-fold higher than pre-drinking values. This compares with a approximately 50-fold increase for the 5-HTOL/5-HIAA ratio in the first morning void. Both methanol and the 5-HTOL/5-HIAA ratio remained elevated above pre-drinking baseline values in the second and sometimes even the third morning voids. Most subjects experienced only mild hangover symptoms after drinking 50 g ethanol (mean score 2.4 +/- 2.6), but the scores were significantly higher after drinking 80 g (7.8 +/- 7.1). The most common symptoms were headache, drowsiness, and fatigue. A highly significant correlation (r = 0.62-0.75, P <0.01) was found between the presence of headache, nausea, and vertigo and the urinary methanol concentration in the first and second morning voids, whereas 5-HTOL/5-HIAA correlated with headache and nausea. These results show that analysing urinary methanol and 5-HTOL furnishes a way to disclose recent drinking after alcohol has no longer been measurable by conventional breath-alcohol tests for at least 5-10h. The results also support the notion that methanol may be an important factor in the aetiology of hangover.

Adult↗
PubMedDate not supplied

Cellular distribution and properties of human blood aldehyde dehydrogenase.

The activity of aldehyde dehydrogenase (ALDH, EC 1.2.1.3) was measured in different fractions of human blood. Of the recovered activity 99% was detected in the intracellular fraction of the erythrocytes. The results also indicated the presence of ALDH activity in the leukocytes, since an increased activity was obtained after cultivation of the cells in the presence of a mitogen. No activity was detected in platelets, plasma, or erythrocyte membranes. Nonlinear Lineweaver-Burk plots were obtained with acetaldehyde, 3,4-dihydroxyphenylacetaldehyde, and indole-3-acetaldehyde as the substrates. The apparent Km values, calculated from the low and high substrate concentration ranges of the curves, were much lower for 3,4-dihydroxyphenylacetaldehyde and indole-3-acetaldehyde than for acetaldehyde. Disulfiram caused almost complete inhibition of the blood ALDH activity in assays with acetaldehyde as the substrate, whereas 15-30% of the activity remained unaffected in assays with 3,4-dihydroxyphenylacetaldehyde and indole-3-acetaldehyde. Kinetic experiments using the mixed substrate method and isoelectric focusing of a partially purified sample of blood did not reveal the presence of more than one isozyme.

Aldehyde Dehydrogenase↗