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The effects of gomisin A, a lignan component of Schizandra fruits, on the promotion stage of hepatocarcinogenesis initiated by 3'-methyl-4-dimethylamino-azobenzene (3'-MeDAB) in male Donryu rats were investigated. When different types of tumor promotors, phenobarbital (PB) and deoxycholic acid (DCA), were administered for 5 weeks after initiation by 3'-MeDAB, preneoplastic alterations in the liver, determined by glutathione S-transferase placental form (GST-P), were markedly increased. Gomisin A significantly inhibited the increase in number and size of GST-P positive foci, regardless of the promotor. This lignan inhibited the increase in serum bile acid concentration by administration of DCA, but hardly influenced the serum bile acids in the PB-combined group. These results suggest that the inhibitory effect of gomisin A on the promotive action of DCA is based on improving bile acid metabolism, but regarding the action of PB, the effect could not be elucidated from the metabolism of bile acids.

We examined the effects of gomisin A on tumor promotion in the liver after a short-term feeding of 3'-methyl-4-dimethylaminoazobenzene (3'-MeDAB) to rats, compared with the effects of phenobarbital. Male Donryu rats were fed ad libitum a diet containing 0.06% 3'-MeDAB and 0.03% or 0.01% gomisin A or water containing 0.05% phenobarbital. Gomisin A and phenobarbital did not cause any pro liferative and neoplastic lesions by themselves in 40 weeks of feeding. Altered foci in the liver increased with a peak at 12 weeks after the rats were fed 3'-MeDAB. Gomi sin A decreased the number of hepatic altered foci such as the clear cell and basophi lic cell type foci in the early stages. Phenobarbital enhanced neoplastic alterations so that the number and size of the foci were much larger in the phenobarbital-combined group than in the 3'-MeDAB-control group. Thus, phenobarbital acted as a promoter of cells initiated by 3'-MeDAB; on the other hand, gomisin A showed a weak sup pressive effect on tumor promotion.

The body temperature in male rats bom to mothers treated with saline or imipramine (5 mg/kg, IMI-F(1)) from day 1 to day 21 of gestation showed a significant decline between 8 and 13 weeks of age. The magnitude of the decline was greater in the IMI-Fi rats than in saline-F, rats. In contrast, the body temperature in the IMI-F, female rats showed a significant rise between 8 and 13 weeks of age. Adult IMI-F(1) male rats showed a significant hyperthermia for 1-2 h after an injection of chlorpromazine while the littermate female rats and the control male and female rats showed a marked hypothermia. The results suggest that prenatal exposure to imipramine induces sex-related alterations in the thermoregulatory centers.