Objective: The purpose of our study was to evaluate the effects of the addition of melatonin and capecitabine on experimental pancreatic cancer.
Methods: Fifty Syrian hamsters were randomized in 5 groups: group 1: no tumor induction (control group); group 2: tumor induction with BOP [N-nitrosobis(2-oxopropyl) amine]; group 3: tumor induction with BOP and melatonin administration; group 4: tumor induction with BOP and capecitabine administration; and group 5: tumor induction with BOP and administration of combined capecitabine and melatonin therapy. The evaluation of pathological tumor evolution and oxidative stress markers in pancreatic tissue was carried out.
Results: All animals under BOP exposure presented poorly or moderately differentiated pancreatic adenocarcinoma associated with increased lipoperoxide levels and decreased antioxidant activity in pancreatic tissue. Pancreatic cancer was shown in only 66% of the capecitabine-treated group and 33% of melatonin-treated group (P < 0.05), most of them moderately differentiated adenocarcinoma. When capecitabine and melatonin were combined, a well-differentiated pancreatic adenocarcinoma was observed in 10% of animals. The beneficial effect was associated with a decrease in lipoperoxide levels and increased antioxidant activity in pancreatic tissue.
Conclusions: The combined administration of capecitabine and melatonin provided an improvement in antioxidant status as well as a synergistic antitumoral effect in experimental pancreatic cancer.
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