Abstract
Depletion of glutathione (GSH) has been proposed as a useful antitumour approach, increasing cellular sensitivity to other anticancer. GSH is a ubiquitous tripeptyde thiol that has a critical role in protection of cells against the cytotoxic effects of a wide variety of drugs, such as activated cyclophosphamide (CY). It has been demonstrated that GSH can protect against the DNA cross-linking effect of this bifunctional alkylating agent, with consequent depletion of intracellular GSH levels. The depletion of GSH content following exposure to activated CY has been attributable to intracellularly released acrolein. Recently, we have shown in studies in vivo , that B16FI0 melanoma cells are sensitive to CY treatment. Thus, high-dose CY therapy (300 mg/kg) significantly ( P P in vitro , the effect of acrolein on GSH levels of Bl6FI0 melanoma cells. We observed that acrulein (10 μM) significantly ( P
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