The effects of dietary carbohydrate on phenobarbital (PB)-, polychlorinated biphenyl (PCB)- or 3-methylcholanthrene (MC)-induced increase in the activity of cytochrome P-450-linked monooxygenase, a UDP-glucuronyltransferase and a glutathione S-transferase in rats were studied. A low-carbohydrate diet increased the monooxygenase activity for all of the hydrocarbons studied (benzene, toluene, styrene, carbon tetrachloride, chloroform, 1, 2-dichloroethane, 1, 1-dichloroethylene and trichloroethylene) without affecting microsomal protein and cytochrome P-450 contents. On the other hand, though causing an increase both in microsomal protein and cytochrome P-450 contents, PB, PCB and MC each produced only a substrate-specific increase in the enzyme activity: PB enhanced the metabolism of toluene, styrene, chloroform and trichloroethylene, but not those of benzene, carbon tetrachloride, 1, 2-dichloroethane and 1, 1-dichloroethylene; PCB increased only the metabolism of toluene, styrene and trichloroethylene; MC did not affect the metabolism of any of the hydrocarbons. A low-carbohydrate diet potentiated the effects of these inducers on the protein and cytochrome P-450, but the augmentation was reflected only in the metabolism of toluene and styrene.Although PB, PCB and MC each increased both activites of UDP-glucuronyltransferase (substrate, p-nitrophenol) and glutathione S-transferase (3, 4-dichloronitrobenzene), the effect of dietary carbohydrate on these transferases was negligible. In addition, a low-carbohydrate diet failed to augment the enhancing effects of these inducers.These results indicate that dietary carbohydrate intake is likely to affect the first phase metabolism of volatile hydrocarbons (functionalization reaction) but is not likely to cause a significant influence on the second phase metabolism (conjugation reactions).