Abstract
The effects of oral supplementation of melatonin on growth of Ehrlich ascites carcinoma (EAC) cells implanted intraperitoneally in female mice were studied. Melatonin at 50 mg/kg body wt. reduced the viability and volume of Ehrlich ascites carcinoma cells and increased the survival of the treated mice. No significant change in intracellular reduced glutathione (GSH) content in EAC cells was observed indicating that GSH was not involved in the inhibitory effect of melatonin. The activity of glutathione- S-transferase in EAC cells was significantly increased. Flow cytometirc studies showed that melatonin not only delayed the progression of cells from G 0/G 1 phase to S-phase of the cell cycle but also reduced DNA synthesis during cell cycle. In addition, the aneuploidy status was depressed in melatonin treated mice. Based on these data and the reduced viability in both in vitro and in vivo, it is suggested that melatonin might induce apoptosis in EAC cells.
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