Abstract
Alcohol and its primary metabolite, acetaldehyde, are central nervous system teratogens. Acetaldehyde can further interact with endogenous biogenic amines under certain conditions to generate tetrahydroisoquinoline (TIQ) alkaloidal metabolites, some of which interfere with adrenergic neuronal function and structural integrity. The possible role of salsolinol (the TIQ derived from the condensation of acetaldehyde with dopamine) in the mechanism of alcohol teratogenicity was investigated in rats. Administration of 2 mg/kg of salsolinol to rats on the 15th day of gestation did not result in the recovery of this TIQ in the fetuses. Furthermore, acute oral administration of alcohol (3 g/kg x 3 doses) to rats on different days of gestation did not result in the synthesis of salsolinol by the fetuses despite the high maternal blood ethanol levels (124 +/- 22 mg%). These findings argue against a role for salsolinol in the mechanism of alcohol teratogenicity. Small amounts of endogenous salsolinol (3.6 ng/g) were detected in fetuses from control rats, in agreement with previous findings in neonatal rats. The physiological role (if any) of endogenous salsolinol in the fetal and neonatal rat is not known.
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