Neuroamine condensations in human subjects.

Non-enzymatic products of neuroamines and endogenous carbonyl compounds are apparent "normal" products in human metabolism, and their levels become increased during pathological conditions. DA condensation products--salsolinol, its O-methylated derivative, and methylated derivatives of 1-carboxyl-THP--are found normally in human urine, and the last TIQ is in human brain. Potential beta-carboline condensation products also occur in (aging) human lens tissue. Chronic drinking in alcoholics causes significant increases in urinary salsolinol and O-methyl-salsolinol, presumably due to the increased AcH which is made available. L-DOPA therapy (in Parkinson's disease) elevates urinary and tissue levels of the carboxylated THP derivatives, as well as of salsolinol and THP itself; hyperphenylalaninemia during PKU also increases tissue levels of a DA/phenylpyruvate-derived TIQ and an imine condensate of phenylethylamine and vitamin B6. These unusual products may interfere with neural dynamic processes, and produce cytotoxic metabolites.