title: Effects of cigarette smoke with different tar contents on hepatic and pulmonary xenobiotic metabolizing enzymes in rats.
abstract: The effects of smoke from cigarettes with two different tar contents (32 mg/cigarette, high tar, and 15 mg/cigarette, low tar) on 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-transferase (GST) activities toward several substrates (1-chloro-2,4-dinitrobenzene [CDNBI; 1,2-dichloro-4-nitrobenzene [DCNB]; ethacrynic acid [EAA]; 1,2-epoxy-3-(p-nitrophenoxy)-propane [ENPP]) were determined in adult male rats. Adult male rats were exposed to smoke of high- or low-tar cigarettes five times a day, with 1-hour intervals, for 3 days in a chamber where smoke and fresh air lead alternatively and were killed 16 hours after the last treatment. Smoke of both high- and low-tar cigarettes (SHTCC and SLTCC) significantly increased hepatic and pulmonary EROD and p-NAOD activities compared to controls. However, the increase noted by SHTCC on pulmonary EROD activity was higher than that of SLTCC. Hepatic AMND and pulmonary AH activities were significantly increased only by SHTCC. LP level was significantly decreased and increased by SHTCC in liver and lung, respectively, whereas it remained unaltered by SLTCC. Only SHTCC significantly increased GSH level in liver. In the lungs, both SHTCC and SLTCC significantly increased GSH level to the same extent. Hepatic GST activity toward EAA was significantly increased by SHTCC but was significantly decreased by SLTCC. ENPP GST activity was significantly decreased by SHTCC and SLTCC in the livers. In the lungs, all the GST activities examined were significantly depressed by SHTCC whereas only GST activity toward DCNB was reduced significantly by SLTCC. These results reveal that the hepatic and pulmonary MOs and GSTs are differentially influenced by SHTCC and SLTCC in rats.
authors.affiliation: Department of Toxicology, Faculty of Pharmacy, Ankara University, Tandoğan, Turkey. eke@pharmacy.ankara.edu.tr
authors.forename: B C
authors.initials: BC
authors.lastname: Eke
authors.forename: M
authors.initials: M
authors.lastname: Işcan
mesh_terms: D000280:Administration, Inhalation; D000818:Animals; D001189:Aryl Hydrocarbon Hydroxylases / Q000096:biosynthesis*; D004305:Dose-Response Relationship, Drug; D004790:Enzyme Induction; D005978:Glutathione / Q000378:metabolism; D005982:Glutathione Transferase / Q000096:biosynthesis; D015227:Lipid Peroxidation / Q000187:drug effects; D008099:Liver / Q000187:drug effects* / Q000201:enzymology*; D008168:Lung / Q000187:drug effects* / Q000201:enzymology*; D008297:Male; D051381:Rats; D017208:Rats, Wistar; D013638:Tars / Q000009:adverse effects* / Q000032:analysis; D014028:Tobacco Smoke Pollution / Q000009:adverse effects* / Q000032:analysis
chemical_list: D013638:Tars; D014028:Tobacco Smoke Pollution; D001189:Aryl Hydrocarbon Hydroxylases; D005982:Glutathione Transferase; D005978:Glutathione