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PubMed1982

Effect of the insecticides toxaphene and carbaryl on induction of lung tumors by benzo[a]pyrene in the mouse.

The insecticides toxaphene and carbaryl, when fed in the diet alone for 20 wk, were not tumorigenic to female A/J mice. Dietary levels of these insecticides were investigated for their effects on the incidence of lung tumors induced by oral administration of benzo[a]pyrene (BP). A significant reduction in BP-induced lung tumors was found after feeding 100 ppm toxaphene for 12 wk or 200 ppm for 20 wk. In contrast, 1000 ppm carbaryl fed for 20 wk caused a significant enhancement of BP-induced lung tumors. Mice that received toxaphene in the diet alone, or toxaphene and BP, showed an increase in BP hydroxylase activity in the liver and a decrease in enzyme activity in the lung. Carbaryl and BP increased BP hydroxylase activity in the lung without altering enzyme activity in the liver. Inhibition of lung BP hydroxylase activity was paralleled by a reduction in BP-induced lung tumors in mice fed toxaphene. Conversely, increased lung BP hydroxylase activity was associated with an enhancement of BP-induced lung tumors in animals fed carbaryl. The metabolism of BP by organs susceptible to BP-induced tumors and possible mechanisms for interactions with the insecticides are discussed.

Animals↗
PubMed1981

Presence of benzo[a]pyrene metabolizing activities in isolated rat liver nucleoli.

A benzo[a]pyrene (B[a]P) hydroxylase activity and epoxide hydrolase (EH) activity have been found in rat liver nucleoli obtained from untreated (C) and 3-methylcholanthrene (3-MC) pretreated rats. A comparison of the enzyme activities was made in rat nuclei and nucleoli. Light and electron microscopic observations of nucleolar preparations did not reveal significant contamination either by intact nuclei or by nuclear membranes, and glucose 6-phosphatase, a marker of microsomal activity, was not detected in our nucleolar preparations. NADPH cytochrome c-reductase could be measured in C and 3-MC nuclei and very low but detectable activity was found in the nucleoli. Nucleolar preparations revealed significant hydroxylating activity, which was inducible by 3-MC in nuclei but not in nucleoli. The presence of EH in nucleoli was demonstrated with phenanthrene 9,10-oxide and B[a]P 4,5-oxide, but the nucleolar activities were lower than those obtained using intact nuclei. The addition of 1,1,1-trichloropropene 2,3-oxide completely inhibited EH activity. Furthermore the presence of covalently-bound metabolites of B[a]P formed in isolated nucleoli was demonstrated by cytofluoromicroscopy.

Animals↗
PubMed1983

The effects of dietary corn oil on the metabolism and activation of benzo[a]pyrene by the benzo[a]pyrene metabolizing enzymes of the mouse.

Male ICR Swiss mice, weighing 16-20 g, were fed ad libitum either a fat-free diet or a diet containing 10% corn oil. After three weeks on these diets, the rates of benzo[a]pyrene (B[a]P) metabolite formation and metabolism to products which covalently bind with macromolecules were compared using hepatic nuclei and microsomal preparations. The maximum activity of B[a]P hydroxylase in microsomes from untreated animals was increased 50% by feeding the corn oil diet, however, B[a]P hydroxylase in microsomes from 3-methylcholanthrene (3-MC)-treated mice was unaffected by diet. In animals treated with phenobarbital, B[a]P metabolism and B[a]P-DNA adduct formation were greater in microsomes from corn oil fed mice compared to those fed the fat-free diet. At a B[a]P concentration of 96 microM, microsomes from corn oil fed untreated mice produced 26% more extractable metabolites and covalent binding to exogenous DNA was increased 46%. At lower substrate concentrations (0.94-15.0 microM B[a]P), B[a]P-DNA and B[a]P-protein binding were 300-400% greater when incubated with microsomes from corn oil fed mice than when incubated with microsomes from mice fed fat-free diet. The apparent Vmax's determined for the formation of each extractable metabolite were increased 1.5-3.0 times by the corn oil diet. Hepatic nuclear B[a]P hydroxylase and nuclear activation of B[a]P to products which covalently bind to DNA in both non-induced and 3-MC-pretreated animals fed the corn oil diet were greater than that observed in animals fed the fat-free diet. B[a]P hydroxylase activities in the lungs of these animals were unaltered by diet.

Animals↗
PubMed1983

A comparison between the activation of benzo[a]pyrene in organ cultures and microsomes from the tracheal epithelium of rats and hamsters.

Epidermoid cancers of tracheal origin produced in Syrian golden hamsters and Fischer strain 344 rats are models for human bronchogenic carcinomas. These two species differ, however, in the sensitivity of their tracheal epithelia to tumor induction elicited by intratracheal benzo[a]pyrene (BP)-ferric oxide administration. The tracheas of hamsters are quite sensitive to the carcinogenic effects of BP-ferric oxide, but rat tracheas are apparently resistant to effects of comparable treatments by this route of administration. Rat tracheas are not completely resistant to polynuclear hydrocarbon carcinogenesis because in the heterotopic tracheal graft model, epidermoid carcinomas have been produced frequently. To determine whether differences in BP metabolism could explain this difference between species, quantitative kinetic and chromatographic studies of benzo[a]pyrene monoxygenase activity were carried out in epithelial microsomes and cells from organ cultures of rat and hamster tracheas. The Vmax was 2-fold greater in hamster tracheal cells than in rat tracheal cells whereas the Km values were identical. H.p.l.c. profiles from microsomes of rat and hamster tracheal epithelial cells incubated with BP exhibited extreme differences. Hamster tracheal microsomes produced large proportions of BP-quinones, BP-phenols, and BP-diols but rat tracheal microsomes produced mostly 3-OH BP. The total metabolic rate for BP in rat tracheal organ cultures was half that in cultures of hamster tracheas. The metabolites isolated in organ cultures of hamster and rat tracheas well reflected secondary reactions of conjugation and recycling. When evaluated with respect to the amount of tissue used, the most striking difference between rat and hamster tracheal organ cultures was in the amount of products which co-chromatographed with bay-region BP-tetrols. The amount of BP-tetrols produced by hamster tracheas was 0.22 pmol/mg tissue/24 h, and by rat, 0.012 pmol/mg tissue/24 h. The level of BP-DNA binding (in pmol/microgram DNA/24 h) catalyzed by hamster tracheal cells was 26.6 +/- 11.4, and by rat tracheas was 1.55 +/- 1.29. These interspecies differences associated with the formation of BP-diol epoxide, a presumed ultimate carcinogenic form of BP, are consistent with the differences between these two rodent species in susceptibility to carcinogenesis in this tissue.

Animals↗
PubMed1981

Enhanced pulmonary and intestinal activation of procarcinogens and mutagens after chronic ethanol consumption in the rat.

Recent epidemiological surveys have indicated that alcoholics exhibit increased incidences of a variety of cancers. We have investigated, as a possible contributing factor to carcinogenesis in this population, the effect of chronic ethanol consumption on metabolic activation of procarcinogens by microsomes isolated from lungs and small intestine. These tissues are major sites through which procarcinogens enter the body and are also potential sites of procarcinogen metabolism. Rat litter-mates were pair-fed nutritionally adequate liquid diets which contained either ethanol as 36% of total energy or an equivalent energy content of carbohydrates in place of ethanol. Chronic ethanol consumption produced significant increases in pulmonary microsomal cytochrome P-450 and microsomal ethanol oxidation. The ethanol diet also enhanced the capacity of pulmonary microsomes to activate compounds present in tobacco pyrolyzates to mutagens detectable in the Ames Salmonella auxotroph reversion assay. The ethanol diet did not alter the capacity of pulmonary microsomes to hydroxylate benzo(a)pyrene (BaP) or to activate BaP to a mutagen. In contrast, microsomes from the upper small intestine of ethanol-fed rats did exhibit both higher levels of BaP hydroxylase activity and enhanced activation of BaP to a mutagen. The ethanol feeding also enhanced the capacity of the intestinal microsomes to activate to mutagens both tryptophan pyrolyzate and 2-aminofluorene but did not influence the metabolic activation of these promutagens by pulmonary microsomes. Chronic ethanol consumption thus influences carcinogen metabolism in the intestine and lung in a manner which varies with respect to both carcinogen and tissue.

Alcoholism↗