Metabolites isolated from the urine of rats after oral administration of beta-myrcene (I) were: 10-hydroxylinalool (II), 7-methyl-3-methylene-oct-6-ene-1,2-diol (IV), 1-hydroxymethyl-4-isopropenyl cyclohexanol (VI), 10-carboxylinalool (III) and 2-hydroxy-7-methyl-3-methylene-oct-6-enoic acid (V). Liver microsomes prepared from phenobarbital-treated rats convert beta-myrcene (I) to 10-hydroxylinalool (II) in the presence of NADPH and oxygen. NADH neither supported this reaction nor did it show any synergistic effect. The rate of conversion was significantly greater in microsomes prepared from phenobarbital-treated rats than from 3-methylcholanthrene-treated or control microsomal preparations. The formation of 10-hydroxylinalool (II) was inhibited by metyrapone, carbon monoxide, SKF-525A, p-chloromercuric benzoate (p-CMB) and cytochrome c. Titration of phenobarbital-induced liver microsomes with beta-myrcene (I) produced a series of type I difference spectra with peaks around 387-390 nm and troughs around 421-425 nm. The Ks for beta-myrcene was 10.6 microM. Administration (four days) of beta-myrcene (I) to rats did not result in any significant effect on the hepatic drug-metabolizing enzymes.