The effects of 3-methylcholanthrene (3-MC), 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), phenobarbital, trans-stilbene oxide (TSO), pregnenolone-16 alpha-carbonitrile (PCN), dexamethasone, ethanol, isoniazid and butylated hydroxyanisole (BHA) on hepatic glutathione S-transferase (GST) activities toward six substrates were determined in hamsters. TCDD and 3-MC, which are comparatively poor inducers of GSTs in rats, were most effective in enhancing GST activities in hamster liver. In contrast, TSO, BHA and phenobarbital, which are very effective inducers of hepatic GSTs in rats and mice, were ineffective or poor inducers of GSTs in hamster liver. While dexamethasone increased some GST activities, treatments with PCN, ethanol and isoniazid were without effect. The findings indicate that not only the control activity but also the inducibility of hepatic GSTs are different in hamsters from those in other species.