The influence of essential oils from naturally occurring plant dietary items such as cardamom, celery seed, cumin seed, coriander, ginger, nutmeg, and zanthoxylum on the activities of hepatic carcinogen-metabolizing enzymes (cytochrome P450, aryl hydrocarbon hydroxylase, and glutathione S-transferase) and acid-soluble sulfhydryl level was investigated in Swiss albino mice. Each oil was fed by gavage at 10 microliters/day for 14 days, and then the animals were sacrificed and their hepatic enzyme activities and sulfhydryl levels were evaluated. Only nutmeg and zanthoxylum oils induced cytochrome P450 level significantly (p < 0.05), whereas cardamom oil caused a significant reduction in its activity (p < 0.05). Furthermore, aryl hydrocarbon hydroxylase activity was significantly elevated only by treatment with ginger oil (p < 0.01), whereas nutmeg oil caused a significant reduction in its activity (p < 0.01). The remaining oils did not significantly alter the level of cytochrome P450 and aryl hydrocarbon hydroxylase activity. Glutathione S-transferase activity was significantly elevated in all experimental groups (p < 0.1-p < 0.001) compared with controls. The acid-soluble sulfhydryl was significantly elevated only by the essential oils of cardamom (p < 0.05), nutmeg (p < 0.05), and zanthoxylum (p < 0.01). Our observations suggest that intake of essential oils affects the host enzymes associated with activation and detoxication of xenobiotic compounds, including chemical carcinogens and mutagens.

The influence of pregnant mare serum gonadotropin (PSGM) on the induction of ovarian tumors by carcinogen(DMBA) and/or mutagens (EMS and BMS) has been studied in Swiss albino mice. Priming of the ovaries of 6-week-old mice with PMSG (50 IU/mouse) 24 h before intragastric intubation of DMBA (5 mg/mouse) resulted in a significant increase in ovarian tumors when harvested 6 months after the treatment. A similar experiment done on 8-week-old mice yielded confirmatory results. Mutagens (EMS and BMS) failed, at given dose levels (200 mg/kg and 300 mg/kg body weight), to induce tumors in normal as well as PMSG-primed ovaries. Pretreatment of animals with PMSG-enhanced DMBA-induced oocyte depletion and also increased the DMBA-3H activity in the ovaries. The augmentation of DMBA-induced tumors in PMSG-primed ovaries could be due to increased uptake of DMBA and increased depletion of oocytes. It is also possible that PMSG-primed ovaries provided more proliferating granulosa cells (and macromolecules) for the interaction of DMBA (or its metabolites) and thereby increased the chances of cell transformation in the ovaries.

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The present communication reports the inhibitory action of aminoglutethimide on 9,10-dimethyl-1,2-benzanthracene (DMBA) induced mammary carcinogenesis in virgin female Holtzman rats. When 20 mg of DMBA is given to the rats and maintained on normal diet for 32 weeks, ∼ 70% of the animals develop mammary tumors. When animals similarly treated with DMBA are put on diets containing 0.025%, 0.05%, and 0.1% of aminoglutethimide for 32 weeks, there is a decline in the number of tumor-bearing animals as well as in the number of tumors per tumor-bearing animal, especially at higher diet doses of the drug. This inhibitory action on the induction of mammary tumors by DMBA could be mainly due to the suppressive action of the drug on endocrine functions.