Celecoxib administration exhibits tissue specific effect on 3H-benzo(a)pyrene-DNA adduct formation in cigarette smoke inhaling mice.

In the present study, cigarette smoke (CS) exposure significantly enhanced 3H-B(a)P-DNA adduct formation in both the pulmonary and hepatic tissues. Mice co-treated with CS and celecoxib (a specific COX-2 inhibitor) exhibited a significant decrease in hepatic carcinogen-DNA adduct formation in comparison to the smoke exposed group, however the lungs of the co-treated animals exhibited a significant increase in carcinogen-DNA adduct formation when compared to the control group and smoke exposed group. CS exposure enhanced the activity of carcinogen activation enzymes in both the tissues and decreased the activity of carcinogen detoxification enzymes in the hepatic tissue only, when compared to the control group. Celecoxib administration to CS inhaling mice modulated the carcinogen biotransformation considerably when compared to the CS exposed group. Celecoxib administration to CS inhaling mice produced a low index of carcinogenesis in the hepatic tissue but increased the index of carcinogenesis in the pulmonary tissue. These observations seem to be critical and tissue specific when related to carcinogenesis.