PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Aniline Compounds”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 109 records · Page 6Linked to original sources
PubMed1983

Effect of butylated hydroxytoluene and butylated hydroxyanisole on the mutagenicity of 3,2'-dimethyl-4-aminobiphenyl.

This study was undertaken to investigate the possible antimutagenic effects of butylated hydroxyanisole (BHA) and butylated hydroxytoluene (BHT) on 3,2'-dimethyl-4-aminobiphenyl (DMAB)-induced mutagenicity, using the Ames Salmonella/mammalian microsome system. The addition of 100-250 micrograms of BHT or 25-500 micrograms of BHA/plate was found to inhibit DMAB-induced mutagenicity in Salmonella strains TA 98 and TA 100. In TA 100, the mutagenicity was further inhibited with the addition of S9 prepared from the livers of rats fed a 0.6% BHT diet as compared to S9 from the animals fed a diet containing no BHT.

Aminobiphenyl Compounds↗
PubMed1981

Effect of dietary wheat bran and dehydrated citrus fiber on 3,2'-dimethyl-4-aminobiphenyl-induced intestinal carcinogenesis in F344 rats.

The effect of dietary wheat bran and dehydrated citrus fiber on 3,2'-dimethyl-4-aminobiphenyl (DMAB)-induced colon and small intestinal carcinogenesis was studied in male F344 rats. Weanling rats were fed semipurified diets containing 5% alphacel, 5% alphacel + 15% wheat bran or 5% alphacel + 15% citrus fiber. At 7 weeks of age, all animals, except vehicle-treated controls, received weekly s.c. injections of 50 mg DMAB/kg body weight for 20 weeks. The DMAB- or vehicle-treated groups were autopsied 20 weeks after the last injection of DMAB. The animals fed the wheat bran diet and treated with DMAB had a lower incidence (number of animals with tumors) and multiplicity (number of tumors/tumor-bearing animal) of colon and small intestinal tumors than did those fed the control diet and treated with DMAB. Animals fed the diet containing citrus fiber developed fewer small intestinal tumors (incidence and multiplicity) than did the rats fed the control diet; the number of adenocarcinomas was reduced in rats fed the citrus fiber diet. This study thus indicates that diets containing wheat bran and citrus fiber reduce the risk for DMAB-induced intestinal cancer and that the protection against colon cancer depends on the type of fiber.

Aminobiphenyl Compounds↗
PubMed1981

The effect of disulfiram on the carcinogenicity of 3,2'dimethyl-4-aminopbiphenyl in Syrian golden hamsters and rats.

3,2'-Dimethyl-4-aminobiphenyl (DMAB) was administered s.c. to Syrian golden hamsters and CDF rats with and without disulfiram in the diet. In a group of male hamsters given only weekly injections of DMAB over a period of 18-22 months, 10 of 25 hamsters developed adenocarcinomas of the small or large intestine. Three had carcinomas in both the large and small intestine, 3 had only colon carcinomas and 4 only small intestinal carcinomas. In the group fed disulfiram and carcinogen, 10 of 25 hamsters developed adenocarcinomas of the colon, but only one carcinoma of the small intestine occurred. Furthermore, the appearance of intestinal tumors was delayed, Urinary bladder carcinomas occurred in both groups exposed to DMAB, with the appearance being slightly delayed in the group also receiving disulfiram. In male rats given DMAB s.c. once a week for 10 months, the addition of disulfiram in the diet reduced the incidence of cancers of the small intestine, similar to the effects of hamsters, but resulted in the occurrence of a small number of bladder cancers. An unusual occurrence was the development of prostatic carcinoma in rats given DMAB.

Aminobiphenyl Compounds↗
PubMed1985

Formation of DNA adducts in vivo in rat liver and intestinal epithelium after administration of the carcinogen 3,2'-dimethyl-4-aminobiphenyl and its hydroxamic acid.

Administration of the 3H-labeled colon carcinogen, 3,2'-dimethyl-4-aminobiphenyl (DMABP) and its hydroxamic acid derivative, N-hydroxy-N-acetyl-DMABP, to male F344 rats resulted in high levels of covalent binding to hepatic and intestinal DNA, RNA and protein. For both compounds, binding to hepatic macromolecules was 2-4 times higher than in the intestine. High pressure liquid chromatographic analysis of the enzymatically hydrolyzed DNA from liver and intestinal epithelium indicated the presence of two carcinogen-DNA adducts: 5-(deoxyguanosin-N2-yl)-DMABP (15%), N-(deoxyguanosin-8-yl)-DMABP (50%), and a decomposition product of the latter (15%). N-acetylated adducts were not detected. When measured after 7 days, all adducts in the intestinal DNA had decreased by 70%, while only a 29% decrease had occurred in the hepatic DNA. To determine if the loss of DMABP products was a consequence of cell turnover or repair, rats were treated with [3H]thymidine and DMABP, and the specific activity of hepatic liver and intestinal DNA was measured. Between 1 and 7 days only a slight decrease in [3H]thymidine content occurred in hepatic DNA as compared with a 95% reduction in intestinal DNA. Thus, the higher rate of DNA synthesis in the intestine versus that in the liver may serve to promote fixation of the initiating lesion and account for the preferential induction of intestinal cancer by DMABP. Furthermore, comparison of these data with metabolic activation pathways reported earlier strongly suggest that N-hydroxy-DMABP is the proximate carcinogenic metabolite of both DMABP and N-hydroxy-N-acetyl-DMABP.

Acetylation↗
PubMed2004

Alkylaniline-hemoglobin adducts and risk of non-smoking-related bladder cancer.

BACKGROUND: Some members of the arylamine family of compounds, specifically 4-aminobiphenyl (ABP), 2-naphthylamine, and benzidine, are established human bladder carcinogens. Cigarette smoking and use of permanent hair dye contribute substantially to current arylamine exposure. Low levels of 4-ABP exposure have been associated with non-smoking-related bladder cancer. Other arylamine compounds coming from as yet unidentified environmental sources may also be human bladder carcinogens. METHODS: We conducted a population-based case-control study in Los Angeles County, California, involving 298 case subjects with bladder cancer and 308 control subjects, who were matched on age, sex, race/ethnicity, and neighborhood of residence. In-person interviews provided information on tobacco smoking and other potential risk factors for bladder cancer. To assess arylamine exposure, levels of arylamine-hemoglobin adducts of nine selected alkylanilines (2,3-dimethylaniline [2,3-DMA], 2,4-DMA, 2,5-DMA, 2,6-DMA, 3,4-DMA, 3,5-DMA, 2-ethylaniline [2-EA], 3-EA, 4-EA) were measured in peripheral blood collected from study subjects. Analysis of covariance and conditional logistic regression methods were used to analyze the relationship between arylamine-hemoglobin adducts and bladder cancer risk. All statistical tests were two-sided. RESULTS: Levels of all arylamine-hemoglobin adducts, with the exception of 2,6-DMA, were higher in smokers than in nonsmokers, and levels of all arylamine-hemoglobin adducts were higher in case subjects than in control subjects. Arylamine-hemoglobin adducts of 2,6-DMA, 3,5-DMA, and 3-EA were all independently, statistically significantly (all P<.001) associated with bladder cancer risk after adjusting for cigarette smoking at the time of blood collection, lifetime smoking history, and other potential risk factors. These adducts were also independently associated with bladder cancer risk when only nonsmokers at time of blood draw were considered (highest quartile versus lowest quartile: 2,6-DMA, relative risk [RR] of bladder cancer = 8.1, 95% confidence interval [CI] = 3.6 to 18.0; 3,5-DMA, RR = 2.7, 95% CI = 1.2 to 6.0; 3-EA, RR = 4.3, 95% CI = 1.6 to 11.6). CONCLUSIONS: Diverse arylamine exposures are strongly associated with bladder cancer risk among nonsmokers. Because arylamines may account for a substantial proportion of bladder cancers among the general population, identification of environmental sources of these compounds is needed.

Aminobiphenyl Compounds↗
PubMed1976

Influence of the oral contraceptive, menstranol, on drug-metabolizing enzymes of female rats in thiamin-supplemented and deficiency states.

The administration of a diet deficient in thiamin results in elevated hepatic microsomal activity of aniline hydroxylase, ethylmorphone demethylase, NADPH cytochrome c reductase and cytochrome P-450 when compared to similar female rats fed diets supplemented with thiamin. Accompanying these differences in enzyme activity are increased concentrations of microsomal docosahexaenoic acid and arachidonic acid. Binding of aniline to microsomes from rats fed high levels of thiamin is decreased due to a decrease in cytochrome P-450. On the other hand, the binding of ethylmorphine to P-450 is decreased by feeding high levels of thiamin. The daily administration of mestranol enhanced ethylmorphine and aniline metabolism to a greater extent in rats fed thiamin-rich diet than in rats fed thiamin-deficient diet or laboratory chow. This treatment did not increase cytochrome P-450 cytochrome c reductase or microsomal protein nor does it appear to affect the binding of aniline to cytochrome P-450. Ethylmorphine binding is generally decreased by this treatment. Alterations in the Michaelis constants for these reactions were limited to an increase in the Ks for aniline in pair-fed animals and in the Ks for ethylmorphine in thiamin-deficient rats receiving 1.0 mg mestranol per day.

Aniline Compounds↗
PubMed1979

Sex-related differences in biotransformation of aniline hydroxylase in Sprague-Dawley rats.

A significant difference was found in the rate of aromatic hydroxylation of the type II substrate, aniline, between male and female rats of the Sprague-Dawley strain. In addition, microsomal cytochrome P-450 levels were significantly lower in female rats and aniline-induced spectral binding was significantly greater in microsomes isolated from male rats. Castration caused a significant reduction in aniline metabolism in male rats and testosterone treatment elevated this metabolism toward control level. Treatment of male rats with 17beta-estradiol significantly reduced aniline hydroxylase activity and female rats receiving testosterone for 1 month exhibited significantly increased rates of aniline metabolism over control females. Enzyme activities measured in immature male and in mature and immature female rats were all significantly lower than in mature male rats. These results suggest that the metabolism of aniline in Sprague-Dawley derived rats is controlled by androgen and, thus, is sex-dependent.

Aniline Compounds↗
PubMed1979

Annual differences in daily variations in hepatic drug metabolizing enzyme activity and plasma hormone levels in the rat.

Daily variations in hepatic drug metabolism and in plasma corticosterone and insulin levels were examined at monthly intervals over the duration of 1 year. Annual differences were observed in the basal levels of all parameters. Consistent daily variations were observed only in plasma corticosterone levels, whereas daily variations in each of the other parameters occurred inconsistently over the year with significant variations being found in ethylmorphine metabolism and insulin levels only five times, and in aniline metabolism, six times. These data show that daily variations in the parameters examined do not occur in a regular manner.

Aniline Compounds↗
PubMed1978

Enhancement in vivo of drug oxidations following administration of benzphetamine, acetone, metyrapone and dimethylsulfoxide.

Effects of benzphetamine, acetone, metyrapone and dimethylsulfoxide administration to rats on the metabolism of drugs by liver 9,000 x g supernatant fraction were studied herein. Activities for aniline hydroxylation and phenacetin O-deethylation were increased while ethylmorphine and benzphetamine N-demethylations were unchanged by the single administration of acetone, metyrapone or dimethylsulfoxide. Increase in aniline hydroxylase activity by about 53.4% and in phenacetin O-deethylase activity by about 44.4% were observed at 30 min after the single administration of benzphetamine whereas ethylmorphine N-demethylase activity was slightly decreased. NADPH-cytochrome P-450 reductase activity and cytochrome P-450 content were unaltered until 12 hr after the single administration of benzphetamine. Aniline hydroxylation was increased by the addition of benzphetamine to the incubation mixture and the increase in aniline hydroxylation caused by benzphetamine could be reversed by washing the microsomes.

Acetone↗
PubMed1983

In vivo metabolism of 3,2'-dimethyl-4-aminobiphenyl (DMAB) bearing on its organotropism in the Syrian golden hamster and the F344 rat.

The in vivo metabolism of tritiated DMAB was examined in male Syrian golden hamsters, which are susceptible to both urinary bladder and intestinal carcinogenesis by this agent and in male F344 rats in which intestinal tumors represent the main lesions. Evidence was obtained for the presence of the N-hydroxy-N-glucuronide of DMAB as a major metabolite in hamster urine and bile and in rat bile but not urine. The routes of excretion of this metabolite, which may represent a transport form of the ultimate carcinogen, correlate well with the main tumor sites in the two species. Other metabolites partially identified were the sulfates and glucuronides of C-hydroxylated DMAB and C-hydroxylated-N-acetyl DMAB.

Aminobiphenyl Compounds↗