Benzo[a]pyrene and nicotine alter prostaglandin E2 receptor and its functions in hamster buccal mucosa

This study investigated the in vivo effect of benzo[a]pyrene (BP) and nicotine (NC) on prostaglandin E2 (PGE2) receptor and its cellular responses in hamster buccal mucosa. Adult male Syrian hamsters were treated by apical swabbing the pouch with mineral oil (control), or 1 mM BP + NC, twice/day, 3 times/week, for 8 weeks. The BP + NC treatment significantly decreased the specific binding of PGE2 to buccal mucosal membranes (12.8 +/- 0.14 vs 8.7 +/- 1.13 fmol/mg protein; control vs. BP + NC; mean +/- S.D., n=6, P < 0.05). Scatchard analysis revealed that the reduction of receptor binding might be due to an alteration of the receptor binding properties, such as increase of the dissociation constant (Kd, 1.08 vs. 4.20 nM; control vs. BP + NC) and elimination of the low-affinity binding site. The addition of 16,16-dimethyl PGE2 (DMPGE2) into the control buccal tissue caused a 36% decrease of the overall protein synthesis. In contrast, DMPGE2 enhanced the [35S]methionine incorporation into several major proteins (i.e., 150, 120, 90, 75, 55, 38 and 26 kDa) in the BP + NC group. DMPGE2 showed no effect on DNA synthesis in both groups. Our data demonstrated that BP + NC in vivo altered PGE2 receptor properties and cellular functions in hamster buccal pouch.