Gender dependent effects of cigarette smoke on hepatic and pulmonary xenobiotic metabolizing enzymes in rats.

The adult male and female rats were exposed to cigarette smoke (CS) 5 times a day, with 1 h intervals, for 3 days in a chamber where smoke and fresh air lead alternatively and were killed 16 h after the last treatments and hepatic and pulmonary monooxygenase (MO) activities (aniline-4-hydroxylase, AH; aminopyrine-N-demethylase, AMND; 7-ethoxyresorufin-O-deethylase, EROD; p-nitroanisole-O-demethylase, p-NAOD), lipid peroxidation (LP) and reduced glutathione (GSH) levels and glutathione-S-transferases (GSTs) activities toward several substrates (1-chloro-2,4-dinitrobenzene, CDNB; 1,2-dichloro-4-nitrobenzene, DCNB; ethacrynic acid, EAA; 1,2-epoxy-3-(p-nitrophenoxy)-propane, ENPP) were determined. CS significantly increased hepatic AMND, EROD and p-NAOD activities whereas it unaltered AH activity in both genders as compared with controls. In the lung, EROD and p-NAOD activities were also significantly increased by CS in both genders. Pulmonary AH activity, however, significantly increased in males but remained unchanged in females. Pulmonary AMND activity significantly increased in females but remained unaltered in males. A significant decrease was noted in the LP level of males, while that of females was unaltered by CS in the liver. Pulmonary GSH and LP, and hepatic GSH levels were significantly increased by CS in both genders. In males, GST activities toward CDNB and DCNB did not alter, whereas GST activities toward EAA and ENPP significantly increased and decreased, respectively, in the liver. In females, CS significantly increased hepatic GST activity toward DCNB but it was ineffective on the other hepatic GST activities. All pulmonary GST activities of males were significantly depressed by CS. In females, however, CS significantly increased pulmonary GST activities toward CDNB and DCNB but was ineffective on GST activities toward EAA and ENPP. These results suggest that gender related differences exist in the modulations of hepatic GST, and pulmonary MO and GST activities but not in those of hepatic MO activities, by CS in rats.