Effects of dietary fish oil (MaxEPA) on N-nitrosobis(2-oxopropyl)amine (BOP)-induced pancreatic carcinogenesis in hamsters

In the present study the chemopreventive potential of 25% fat (HF) diets containing 2 wt% linoleic acid (LA) and including 0.0, 1.2, 2.4, 4.7, 7.1 or 9.4 wt% dietary fish oil (MaxEPA) has been investigated using the N-nitrosobis(2-oxopropyl)amine (BOP)-hamster model for pancreatic cancer. The number of pancreatic borderline lesions (BLL) was significantly higher (P < 0.05) in the HF groups containing 1.2, 2.4 or 9.4 wt% MaxEPA in comparison with the HF group without MaxEPA. MaxEPA inhibited the metabolism of LA to arachidonic acid (AA) and of AA to prostaglandins (PGs) in both blood plasma and pancreatic microsomes. The pancreatic levels of PGE2 (P < 0.05), 6-keto-PGF1α (P < 0.01) and PGF2α (P < 0.05) decreased significantly with increasing dietary MaxEPA. The levels of PGE2 (P < 0.001), 6-keto-PGF1α (P < 0.05), PGF2α (P < 0.001) and thromboxane (TX) B2 (P < 0.001) in pancreatic adenocarcinomas were higher than in nontumorous pancreas. The MaxEPA had no significant effect on the BrdU labeling index (LI) in acinar, ductular or centroacinar cells, nor on the LI in BOP-induced pancreatic lesions. It is concluded that (i) dietary fish oil has a slight enhancing effect on BOP-induced pancreatic carcinogenesis in hamsters and (ii) dietary fish oil dose-dependently inhibits the conversion of LA to AA and of AA to certain PGs and (iii) dietary fish oil does not influence the cell proliferation in hamster pancreas.