Endogenous induction of transient oxidant-imbalances in Ehrlich cells as a possible trigger to fast tumor fluid accumulation.

During the Ehrlich ascitic carcinoma (EAC) development in vivo, we found the stage that had the transient imbalance between the increased activity of H2O2-producing enzyme superoxide dismutase (SOD) and the low activity of H2O2-removing enzyme glutathione peroxidase (GSH-Px). The appearance of this oxidant imbalance closely correlated with fast ascitic fluid accumulation in peritoneal cavity and the appearance of an EAC cell subpopulation which contains individual sites with high receptivity to endogenous reduction of paranitroviolet tetrazolium (PNVT). Surprisingly, PNVT-reducted sites have been found to be located on the surface of the EAC intracellular lipoprotein granules. To account for these facts, we suggest that the appearance of the stage with a transient tumor oxidant imbalance may act as a trigger for fast fluid influx to the tumor through increased blood vessel permeability, as well as a protector of hypoglycemic EAC cells via H2O2-dependent increase of glucose intracellular delivery (in a manner similar to insulin).