This study was supported by the Bundesministerium fuer Forschung und Technologie (Grant BMFT 07NBL07/6).
Plasma and Urine Salsolinol in Humans: Effect of Acute Ethanol Intake on the Enantiomeric Composition of Salsolinol
Article first published online: 11 APR 2006
Alcoholism: Clinical and Experimental Research
Volume 20, Issue 1, pages 87–92, February 1996
How to Cite
Haber, H., Winkler, A., Putscher, I., Henklein, P., Baeger, I., Georgi, M. and Melzig, M. F. (1996), Plasma and Urine Salsolinol in Humans: Effect of Acute Ethanol Intake on the Enantiomeric Composition of Salsolinol. Alcoholism: Clinical and Experimental Research, 20: 87–92. doi: 10.1111/j.1530-0277.1996.tb01049.x
- Issue published online: 11 APR 2006
- Article first published online: 11 APR 2006
- Received for publication July 22, 1995; accepted September 5, 1995
- Gas Chromatography/Mass Spectrometry
The tetrahydroisoquinoline (TIQ) salsolinol (SAL), a condensation product of dopamine and pyruvate or acetaldehyde, is one of the neuropharmacologically active alkaloids in mammals. Previous HPLC studies have shown that the R-enantiomer of SAL is largely predominant, or is the only enantiomer in the urine of healthy subjects, whereas the S-enantiomer was found predominant in the urine of alcoholics. An enzymatic pathway for SAL formation that is influenced by chronic alcohol intake was proposed. However, our analyses showed that the SAL detectable in human urine and plasma is racemic, at least in healthy subjects. No change of the enantiomeric distribution was observed after an acute alcohol ingestion (1 g alcohol/kg body weight). Using a new method for the resolution of the SAL enantiomers and gas chromatography/mass spectrometry analysis, the SAL enantiomers were quantified in the urine and plasma of 24 subjects before and after the intake of alcohol. Special dietary conditions were observed to avoid interferences by the SAL of the foodstuff. Although the distribution of SAL enantiomers was not changed after alcohol intake, the total urinary SAL output and the plasma concentration of SAL were significantly influenced in different ways. Only five subjects showed a significant increase both in plasma SAL concentration and in the total urinary SAL output, whereas 19 subjects showed decreased or unchanged SAL levels after alcohol administration. Data also show that only the subjects with low baseline levels (mean of 0.148 ng SAL/ml plasma) tend to increase SAL levels after ethanol ingestion, which may imply some genetic basis for the response.