Effects of benzene and other organic solvents on the decarboxylation of some brain aromatic-L-amino acids.

The intraperitoneal administration of benzene produced marked increases in mouse striatal concentrations of beta-phenylethylamine, p-tyramine and, to a lesser extent, m-tyramine. Similar increases were observed in rat striatal p- and m-tyramine. The subcutaneous administration of benzene dissolved in sesame oil increased mouse striatal p-tyramine but did not change m-tyramine. Benzene administration to mice pretreated with p-tyrosine produced marked increases in mouse striatal p-tyramine as well as in m-tyramine. The statistical analysis of the results indicated that the treatment produced an interaction that led to an increase in the concentration of both the p- and m-isomers of tyramine. The administration of benzene to m-tyrosine-pretreated mice increased striatal m-tyramine but p-tyramine was not increased. The treatment produced no potentiation in the formation of p- or m-tyramine. Of the other organic solvents given, pyridine produced the most marked effects. Its administration increased the concentration of both p- and m-tyramine in the mouse striatum. Treatment with toluene, chloroform, carbon tetrachloride or isoamylalcohol produced moderate increases in mouse striatal p-tyramine while toluene, dichloromethane or isobutylalcohol also increased m-tyramine. These increases in brain beta-phenylethylamine, p-tyramine and m-tyramine may play a contributory role in the human toxicity of benzene and some of these organic solvents; these toxic effects could be exacerbated after ingestion of foodstuffs containing the aminoacids phenylalanine or p-tyrosine or for those under treatment with a monoamine oxidase inhibitor.