Long-term caffeine-induced inhibition of EAC cell progression in relation to gonadal hormonal status.

Inhibitory action of caffeine (a tri-methylxanthine alkaloid) on progression or pathogenesis of lung, breast and ovarian cancer including Ehrlich ascites carcinoma (EAC) cell development has been reported. This information led the authors to study the effect of long-term administration of caffeine (20 mg/kg/day; po for 22-27 consecutive days) on the development of EAC cells in relation to serum gonadal hormones (LH, FSH, 17-OH-beta-estradiol (E2) and progesterone) in adult Swiss albino female mice. Measurement of gonadal hormones in serum using RIA showed that (a) long-term caffeine treatment significantly increased LH (except for 27 consecutive days) and decreased FSH (except for 24 and 27 consecutive days) and both E2 and progesterone (except for 22 and 24 consecutive days) levels, (b) development of EAC cell for 10-15 days, significantly increased LH but decreased FSH, E2 and progesterone levels and (c) long-term caffeine consumption during the development of EAC cell (i) restored the EAC cell- or caffeine-induced induction of LH and reduction of FSH level to their normal levels and (ii) withdrew/reduced the EAC cell-induced reduction in only E2 but not progesterone level. These results therefore, suggest that prolonged caffeine exposures may inhibit the development of EAC cell through the reduction or restoration of EAC cell-induced disruption of ovarian hormonal status to their normal status via the modulation of Hypothalamic-Pituitary-Gonadal (HPG) axis.

Chronic administration of caffeine: effect on the activities of hepatic antioxidant enzymes of Ehrlich ascites tumor-bearing mice.

Chronic ingestion (for 22-30 consecutive days) of caffeine (20 mg/kg/day, p.o.) increased the activities of the hepatic enzymes- catalase (CAT) and superoxide dismutase (SOD) and decreased its lipid peroxidation (LP) in mice. Development of Ehrlich ascites carcinoma (EAC) cell decreased the activities of hepatic CAT and SOD and increased LP. But pretreatment of caffeine for 12 consecutive days and continuation of its treatment during the course of development of EAC cells restored the EAC cell-induced changes in liver CAT, SOD and LP to their corresponding control values. Thus, the present results by confirming the results of others previously published, suggest that caffeine is an antioxidant and may act as an anticarcinogen.