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At least 19 recordsLinked to original sources
PubMed1991

Exposure to the carcinogen benzopyrene depletes tissue vitamin A: beta-carotene prevents depletion.

Evidence in humans and laboratory animals supports a cancer-protective effect of vitamin A, but the mechanism remains unclear. While vitamin A deficiency causes squamous metaplasia, and lung cancer patients have lower vitamin A status, their serum vitamin A levels are not indicative of deficiency. We hypothesize that local enzymatic degradation of vitamin A can be induced by exposure to carcinogens such as benzopyrene found in cigarette smoke. This study was designed to determine if benzopyrene exposure depletes tissue vitamin A and whether beta-carotene might prevent the depletion. Weanling male Fischer rats were fed a nutritionally complete purified diet, supplemented with or without benzopyrene at 400 mg/kg feed or beta-carotene at 2 g/kg feed. Vitamin A content of the liver, small intestine, and serum was determined by high-performance liquid chromatography. There was no effect of benzopyrene feeding on serum retinol levels through four weeks. However, there was a decline in tissue retinol in the liver and small intestine by two weeks, with a 30% decline by four weeks (p less than 0.05). In rats fed beta-carotene, there was no effect of benzopyrene on tissue vitamin A level. These results indicate that exposure to benzopyrene induces a local tissue vitamin A depletion despite a vitamin A-sufficient diet and maintenance of serum vitamin A levels. A high intake of beta-carotene prevented the vitamin A depletion effect of benzopyrene exposure. Further studies appear warranted to determine whether some of the adverse effects of environmental carcinogens, as found in cigarette smoke, charcoal-broiled meats, and industrial wastes, might be alleviated by dietary intervention.

Analysis of Variance↗
PubMed1982

Acceleration of the development of benzopyrene-induced skin cancer in mice by microwave radiation.

Development and growth of skin cancer may be affected by various physical and chemical factors present in human environment. Of these factors electromagnetic radiation of radio- and microwave spectra are among the most common. In the present study Balb/c mice were exposed to chemical carcinogen, 3,4-benzopyrene, painted on the skin every 2nd day for a total of 6 months, and simultaneously irradiated with athermal (5 mW/cm2) or subthermal (15 mW/cm2) doses of 2,450 MHz microwaves. The other group of animals was preirradiated with microwaves at 10 mW/cm2 power level for 1, 2, or 3 months and then treated with benzopyrene, as above. Control mice were exposed for 6 months to benzopyrene, resulting in the development of baso- or spinocellular skin carcinoma within approximately 9 months, and sham-irradiated with microwaves. The growth of the tumour was assessed according to a self-designed 7-range macroscopic scale, supported by microscopical examinations of skin sections. All protocols of microwave irradiations resulted in a significant acceleration of the development of benzopyrene-induced skin cancer and in shortening of life span of the tumour-bearing hosts. This effect seemed to be dose-dependent since subthermal doses (15 mV/cm2) and longer (3 months) expositions to microwaves were more efficient as compared to athermal doses (5 mW/cm2) and shorter preirradiations. In addition, low-level, long-lasting exposure to microwaves led to a marked suppression of delayed hypersensitivity of mice treated with benzopyrene, as assessed by their reactivity to dinitrofluorbenzene (DNFB). It is suggested that the observed co-carcinogenic effect of microwave radiation may, at least in part, result from the inhibitory action of microwaves on cellular immune reactions of exposed animals.

Animals↗
PubMed1969

Enzymatic hydroxylation of benzopyrene and its relationship to cytotoxicity.

Aryl hydrocarbon hydroxylase, an inducible microsomal enzyme system, has been measured in cultures of normal and transformed hamster, mouse, and human cells. In order to determine the highest level of enzyme, the cells were induced by pretreatment with benz(a)anthracene. A correlation was found between the level of enzyme activity and the susceptibility of the cells to the cytotoxicity produced after treatment with benzopyrene. The results indicate that aryl hydrocarbon hydroxylase is the enzyme system responsible for cell susceptibility to the cytotoxic effect of benzopyrene and the toxic effect of benzopyrene is due to its enzymatic conversion to a cytotoxic metabolite. 3-Hydroxybenzopyrene, one of the products of the enzymatic hydroxylation of benzopyrene, was found to be cytotoxic to cells that were either susceptible or resistant to the cytotoxic effect of benzopyrene.

Animals↗
PubMed1974

Nicotine inhibition of the metabolism of 3,4-benzopyrene, a carcinogen in tobacco smoke.

A decreased rate of biliary excretion of radioactive metabolites of 3,4-benzopyrene was observed in rats given a single dose of nicotine. Prior treatment of rats with nicotine decreased benzopyrene hydroxylase activity in homogenates of liver, lung, and small intestine. The addition of nicotine to incubated tissues also decreased benzopyrene hydroxylase activity. These findings show that nicotine inhibits the metabolism of 3,4-benzopyrene in vivo and in vitro.

Animals↗
PubMed1983

Interactions of chrysotile and benzopyrene in a human cell culture systems.

The risk of lung cancer related to asbestos exposure has been shown to increase disproportionately by cigarette smoking, suggesting a synergistic effect. Differing lengths of NIEHS chrysotile with benzopyrene [B(a)P, B(e)P] (organic by-products of combustion) were applied on normal human fibroblasts (cell line CI) to test for cytotoxicity (survival determined by colony-forming efficiency), binding of benzopyrene to DNA, and the production of benzopyrene metabolites. At concentrations of 100 micrograms/mL, NIEHS short chrysotile was more cytotoxic than NIEHS intermediate chrysotile (3% and 17% survival, respectively); B(a)P and B(e)P concentrations up to and including 10 microM were not cytotoxic. Simultaneous application of NIEHS short chrysotile with B(a)P or B(e)P did not decrease survival synergistically. On the contrary, application of B(a)P simultaneously with NIEHS intermediate chrysotile resulted in increased survival over that of intermediate chrysotile alone (25% and 17% survival, respectively). There were low levels of B(a)P bound to DNA in the presence of NIEHS short chrysotile or NIEHS intermediate chrysotile. Measurable levels of B(a)P-DNA adducts were formed both in the absence and in the presence of each size of NIEHS chrysotile. However, there was no strong indication of a perturbation of the level of DNA-B(a)P binding following simultaneous administration of increasing levels of asbestos in addition to 1 microM hydrocarbon. The asbestos had no demonstrable influence on the level of B(a)P metabolism during the 24-hr period following simultaneous exposure of asbestos and hyrdocarbons.(ABSTRACT TRUNCATED AT 250 WORDS)

Asbestos↗
PubMed1978

Increase of urinary putrescine in 3,4-benzopyrene carcinogenesis and its inhibition by putrescine.

A significant increase in putrescine was noted in the urine of mice with experimental s.c. tumors induced by a single injection of 3,4-benzopyrene solution (2.52 mg of 3,4-benzopyrene in 0.5 ml of tricaprylin). When 10 mg of putrescine were added to the 3,4-benzopyrene solution, the development of tumors was completely inhibited and the increase of urinary putrescine in mice was suppressed simultaneously. Animal weight data of a control group receiving only putrescine indicated that the inhibitory effect of putrescine is not due to its toxicity.

Animals↗
PubMed2006

Effects of benzopyrene-7,8-diol-9,10-epoxide (BPDE) in vitro and of maternal smoking in vivo on micronuclei frequencies in fetal cord blood.

Up to 20% of pregnant women smoke and there is indirect evidence that certain tobacco-specific metabolites can cross the placental barrier and are genotoxic to the fetus. The presence of micronuclei results from chromosome damage and reflects the degree of underlying genetic instability. Fetal blood was obtained from the cord blood of 143 newborns (102 from nonsmoking mothers and 41 from mothers smoking >10 cigarettes/d during pregnancy). The micronucleus assay was performed following the guidelines established by the Human MicroNucleus project with modifications. To test the micronucleus assay, we evaluated the effect of a range of benzopyrene-7,8-diol-9,10-epoxide concentrations (from 3.125 nM to 4 microM) on cord blood from nonsmoking mothers. This validation showed that the number of micronuclei and apoptotic cells increased with benzopyrene-7,8-diol-9,10-epoxide dose (p < 0.0001 and p = 0.001, respectively); the minimal detectable effect was induced by 12.5 nM benzopyrene-7,8-diol-9,10-epoxide. In our sample, the number of MN was significantly higher in the 41 cord blood samples from mothers who smoked during pregnancy [smokers: 4 (1; 10.5); nonsmokers: 3 (0; 8); p = 0.016]. Therefore, the data reported herein support the hypothesis that tobacco compounds are able to induce chromosomal losses and breaks that are detectable as an increased number of micronuclei.

7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide↗
PubMed1980

Oxidation and subsequent glucuronidation of 3,4-benzopyrene in everted intestinal sacs in control and 3-methylcholanthrene-pretreated rats.

The metabolism of 3,4-benzopyrene in the wall of isolated everted intestinal sacs was studied in control and 3-methylcholanthrene induced rats. The luminal (outer) side of the intestine was perfused with a 100-mumol/l concentration of 3,4-benzopyrene in Krebs-Ringer's bicarbonate buffer supplemented with 5% glucose and 2% albumin. A thin-layer chromatography assay method was used to analyze benzo(a)pyrene metabolites. After the pretreatment of rats with 3-methylcholanthrene, the amount of hydroxylated metabolites was about 1.5-fold and the amount of consequent glucuronides was about 3-fold in comparison with the controls. 3-Methylcholanthrene induction mainly increased the production of 3- and 9-hydroxybenzopyrene and dihydrodiols. The glucuronidation of 3- and 9-hydroxybenzopyrene was enhanced by 3-methylcholanthrene but the conjugation of dihydrodiols was nonresponsive to induction. Only small amounts of glucuronides were present in the inner (serosal) side of the intestinal sac. The data suggest different responses of various benzo(a)pyrene metabolites to induction in the intestinal mucosa. In addition to metabolic functions the intestinal mucosa may function as an excretory organ for polycyclic aromatic hydrocarbons entering the body.

Animals↗
PubMed1979

[Eventual presence of 3-4 benzopyrene in the non-saponificable part of sunflower oil].

Within the limit of the research on the chemical composition of the nonsaponds of the edible oils, under execution in our Institute have been affected some cromatografic gas and spectoskopic analysis (U.V.) on a sample of sunflower seeds oil. Concentrating our research essentially on the determination of the presence of 3-4 benzopyrene in the above oil, we have treated about 8,3 gr. of nonsapond with appropriate chemical methodologies, in order to obtain specific samples for the polycyclic aromatic hydrocarbon analysis. The results of the cromatografic gas and spectoskopic of two fractions, obtained through the process of the preparation of the nonsapond sample, compared with those of a standard solution of 3-4 benzopyrene, exclude the presence of the hydrocarbon in the sunflower oil.

Benzopyrenes↗
PubMed1978

[Survey of contamination of food by 3, 4-benzopyrene. I. Demonstration of a universal method of determination. Application to the determination in complete meals in food emporia].

A versatile spectrofluorimetric method is proposed for the determination of 3,4-benzopyrene in foods and biological material. Recording the emission spectrum allows a reliable identification, and determination at a 0,2 ppb level, with 85 p. 100 recovery and good reproductibility. The time required for analysis is decreased, if compared to existing methods. As a test of its reliability, results of a survey on 3,4-benzopyrene content in canteen meals are presented. The values obtain are very low, generally below 1 ppb; their significance is discussed.

Animals↗
PubMed2000

Effect of 3,4-benzopyrene on ultrastructure of sinusoidal cells of the liver in adult male rats.

Reorganization of sinusoidal cells (endotheliocytes, Kupffer cells, and Ito cells) in the liver microregion of male rat liver exposed to 3,4-benzopyrene was studied. Synchronous activation of the lysosome-vacuole systems in Kupffer cells and endotheliocyte indicates cooperation of these cells in detoxification of benzopyrene and its metabolites. Ito cells lose lipid inclusions and actively proliferate; the appearance of intermediate forms between lipocytes and fibroblasts attests to activation of fibrogenesis in the liver.

Animals↗
PubMed1976

The effects of benzopyrene and safrole on biphenyl 2-hydroxylase and other drug-metabolizing enzymes.

A study was made of the nature and specificity of the increase in biphenyl 2-hydroxylase activity after preincubation of liver microsomal preparations with various carcinogens in vitro. This enhancement of enzyme activity in vitro was investigated in mouse, hamster and rat, and although the rat appears to be atypical in the variation of the pattern of 2- and 4-hydroxylation with age, similar enhancements were detectable in each species examined. An increase in biphenyl 2-hydroxylase activity was apparent 2h after intraperitoneal administration of safrole or benzopyrene to mature Wistar albino rats and appeared to be similar in nature to that observed after preincubation of liver microsomal preparations with the same chemical in vitro. Investigation of other drug-metabolizing enzyme systems suggests that the enhancing effects of carcinogens in vitro are specific for biphenyl 2-hydroxylase. No correlation between the enhancement of biphenyl 2-hydroxylase and inhibtion of biphenyl 4-hydroxylase was apparent.

Acetone↗