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N Sera

Publications and source records attributed to N Sera.

At least 37 records · Page 2Linked to original sources
PubMed1998

Comparative tumorigenicity of 1- and 3-nitrobenzo[a]pyrenes, and 3,6- and 1,6-dinitrobenzo[a]pyrenes in F344/DuCrj rats.

Our earlier study revealed that 1- and 3-nitrobenzo[a]pyrene (NBP), 1,6- and 3,6-dinitrobenzo[a]pyrene (DNBP), nitrated derivatives of benzo[a]BP (BP), are present in the environment. These derivatives are potent mutagens for Salmonella tester strains and we have preliminarily reported them to be carcinogenic in F344/DuCrj rats. In this study, the tumorigenic action of 1- and 3-NBP, 1.6- and 3,6-DNBP, and BP induced by subcutaneous injection into rats was found to differ according to the NO2-substitution in the BP structure. The chemicals were suspended in equal volumes of beeswax and tricaprylin, and rats were subcutaneously injected with single doses of 500, 1000, and 2000 microg for 1- and 3-NBP, and of 8, 40, 200, and 1000 microg for 3,6- and 1,6-DNBP, and BP as a positive control. 3,6-DNBP and BP induced tumors in a dose-dependent manner at the injection site. Rats given 1000 microg of 3,6-DNBP (2924 nmol) and BP (3968 nmol) developed subcutaneous tumors at the rate of 70 and 80%, respectively, and those given a minimum dose of 23 nmol for 3.6-DNBP and 32 nmol for BP per rat developed tumors at a rate of 4.8 and 18.2%, respectively. However, rats given 500 and 1000 microg of 1- and 3-NBP did not develop any tumors while those given a high dose, 2000 microg, of each chemical developed tumors at only one of ten animals used. It was concluded, therefore, that these chemicals are weak carcinogens. Histologically, most of the tumors were malignant fibrous histiocytomas. Rats given various doses of 1,6-DNBP did not develop any tumors at the injection site. The failure of 1,6-DNBP to induce tumors may involve its metabolites because of the lower mutagenicity of its reduction products, 1-nitroso-6-NBP and 1-amino-6-NBP. It is suggested, therefore, that tumorigenicities of NBPs and DNBPs differ according to the NO2-substitution on the chemical structure, which may be due to the possible nitroreduction of the chemicals.

Animals↗
PubMed1998

Preoperative treatment of growth hormone-producing pituitary adenoma with continuous subcutaneous infusion of octreotide.

Preoperative therapy with octreotide, a long-acting somatostatin analog, suppresses GH hypersecretion, shrinks GH-producing tumors and leads to an improvement in subsequent surgical remission in acromegalic patients. A continuous infusion of octreotide has demonstrated more persistent suppression of GH secretion than intermittent injections, and only a few studies were reported on the effect of the tumor shrinkage with a continuous infusion of a small dose of octreotide. We therefore investigated the preoperative effects of small doses of octreotide (120-240 micrograms/day) administered continuously (with a subcutaneous infusion pump) over a short period (2 or 4 weeks) in nine untreated acromegalic patients. Octreotide therapy resulted in suppression of serum GH and IGF-1 concentrations in 8 out of 9 patients and reduction in pituitary tumor size measured by MRI in all patients (by 7.9 to 38.5%). In particular, considerable reduction in tumor size (more than 20%) occurred in 6 of 9 patients. In three patients assessed serially throughout the preoperative period, reduction in tumor size was noted within only one week after the start of octreotide therapy and reduction rate more than 20% was obtained within the first two weeks. In one patient, suprasellar tumor expansion totally disappeared after such therapy. Our results indicate that short-term continuous subcutaneous infusion of a small dose of octreotide results in not only inhibition of GH hypersecretion but also shrinkage of tumor size prior to surgery.

Adenoma↗
PubMed1997

beta-Adrenoreceptor antagonistic actions and mutagenicities of R(+)- and S(-)-enantiomers of N-desisopropylpropranolol and its N-acetyl conjugate.

Enantiospecific acetyl conjugation was examined in the rat liver 105000 x g supernatant (cytosol) system using racemic 1-amino-3-(1-naphthyloxy)-2-propanol (NDP), a N-desisopropyl metabolite of propranolol. From the results of chiral separative determination of the samples by HPLC using a Chiralcel OD-R column, more remarkable enantiospecificity was observed in the R(+)-enantiomer on NDP elimination and N-acetyl conjugate (AcNDP) formation. Next, the strength of beta-adrenoceptor antagonistic actions and mutagenicities was compared between R(+)- and S(-)-enantiomers of NDP and AcNDP, respectively. In the case of NDP, both enantiomers possessed weak beta1-adrenoceptor antagonistic effects on isoproterenol-induced positive inotropic and chronotropic actions in the left and right atria isolated from a guinea pig. These actions of R(+)- and S(-)-NDP were 1700-times and 100-times less potent, respectively, than those of propranolol. beta2-Adrenoceptor antagonistic actions of R(+)- and S(-)-NDP in the trachea were 1600-times and 200-times less potent, respectively, than those of propranolol. Enantiospecificity was observed in the beta-adrenoceptor antagonistic action of S(-)-NDP, while R(+)-NDP and both enantiomers of AcNDP appeared to be negligible in this action. On the other hand, the mutagenicities of each enantiomer were examined by the Ames method using 13 kinds of Salmonella typhimurium strains. In the case of AcNDP, the numbers of colonies increased according to the substrate concentration only when rat liver 9000 x g supernatant fraction (S-9 mixture) was added to the plates containing TA100, YG1029, TA104 and YG3003, and then enantiospecificity was observed in the mutagenicity of S(-)-AcNDP. Thus, the ultimate mutagen might be an active metabolite formed mainly from S(-)-AcNDP. Despite of the addition of rat liver S-9 mixture, R(+)-AcNDP and both enantiomers of NDP did not indicate mutagenicity.

Adrenergic beta-Antagonists↗
PubMed1997

Possible role of indoor environment and coal combustion emission in lung carcinogenesis in Fuyuan County, China.

Fuyuan Country, in Yunnan Province, China has an extremely high lung cancer mortality both in males and non-smoking females. Out of 5768 deaths, 588 patients died of malignant diseases. Lung cancer was the number one cause of death among malignant diseases both in males and females. The rate of lung cancer death to the whole of malignant diseases was 56.2% for males and 55.0% for females. Indoor soot and combustion emission derived from smoky coal produced in northern Fuyuan exhibited high mutagenic activities against Salmonella typhimurium TA98 strain in Ames test. Resected lung tissues derived from the patients with lung cancer in Fuyuan contained significantly higher concentrations of benzo(a)pyrene than those in Japan, both in males and females (i.e., 608.7 +/- 477.1 pg/dry weight for samples of the patients in Fuyuan, 180.1 +/- 104.5 for Japanese non-smokers, and 207.5 +/- 98.8 for Japanese heavy smokers, respectively). These results suggest that mutagenic chemicals contained in coal as well as indoor environment may have a great influence on lung carcinogenesis in Fuyuan, Yunnan Province, China.

Air Pollution, Indoor↗
PubMed1996

Mutagenicity of nitrophenanthrene derivatives for Salmonella typhimurium: effects of nitroreductase and acetyltransferase.

To determine the mutagenicity of nitrophenanthrenes, three mononitrophenanthrenes (NPhs), 11 dinitrophenanthrenes (diNPhs) and eight trinitrophenanthrenes (tiNPhs) were synthesized, and their mutagenicity was investigated by using Salmonella typhimurium his- strains TA98, TA100, and TA98NR, nitroreductase-deficient, and TA98/1,8-DNP6, O-acetyltransferase-deficient mutants, and strains YG1021 and YG1026, nitroreductase-overproducing mutants of TA98 and TA100, respectively, and strains YG1024 and YG1029, O-acetyltransferase-overproducing mutants of TA98 and TA100, respectively. 1-, 3- and 9-NPhis induced 329, 620 and 438 revertants per nmol in strain TA100, respectively, and 4,839, 11,309 and 16728 revertants per nmol, respectively, in strain YG1029. Mutagenicity of 1,6-, 2,6-, 2,9-, 2,10-, 3,5-, 3,6- and 3,10-diNPh was elevated in strains YG1021, YG1024, YG1026 and YG1029. Among these derivatives, 1,6-, 2,6-, 3,6- and 3,10-diNPhs were more mutagenic in strains YG1024 and YG1029 than YG1021 and YG1026, and they showed a structure-activity relationship between mutagenicity and NO2-substitution. Nitro derivatives substituted at the 3 and 6 positions of their chemical structure strongly mutated both strains YG1024 and YG1029, whereas those substituted at the 9 and 10 positions showed weak mutagenicity. In addition, nitro substituents at positions 4 and 5 were perpendicular while those on positions 2,3,6 and 7 were nearly coplanar to the aromatic ring. Furthermore, 2,6,9-, 3,6,9- and 1,6,9-trinitrophenanthrenes (triNPhs) were mutagenic for strain TA100, and their mutagenicity was more enhanced in YG1024 and YG1029 than in YG1021 and YG1026. Of the eight triNPhs all except 1,5,10-triNP were mutagenic in TA98 and TA100, and their mutagenicity was more enhanced in YG1024 and YG1029 than in YG1021 and YG1026. These results suggest that these compounds are mutagens that are activated by O-acetyltransferase esterification following nitroreductase. The nitrated derivatives substituted at the 2(7) and 3(6) positions of the phenanthrene ring were highly mutagenic. The relationship between chemical structure and the mutagenicity of NPh derivatives is discussed.

Acetyltransferases↗
PubMed1996

Mutagenicity of the fullerene C60-generated singlet oxygen dependent formation of lipid peroxides.

Fullerene C60 dissolved in polyvinylpyrrolidone was mutagenic for Salmonella strains TA102, TA104 and YG3003 in the presence of rat liver microsomes when it was irradiated by visible light. The mutagenicity was elevated in strain YG3003, a repair enzyme-deficient mutant of TA102. The mutation was reduced in the presence of beta-carotene and parabromophenacyl bromide, a scavenger and an inhibitor, respectively, of phospholipase. The results suggest that singlet oxygen was generated by irradiating the C60 by visible light and that the mutagenicity was due to oxidized phospholipids in rat liver microsomes. Of the phospholipids in rat liver microsomes, the linoleate fraction isolated by high performance liquid chromatography was a major component, and played an important role in mutagenicity. Methyl linoleate, which was prepared for gas chromatographic analysis, was readily oxidized to hydroperoxymethyl linoleate, and associated with both 10- and 12-hydroxyl derivatives with a double bond in chemical structure by singlet oxygen: radicals to the hydroxyl function were probably generated. Because of the instability of the hydroxymethyl linoleate radicals, guanine residues generated radicals. The results of ESR spectrum analysis suggested generation of radicals at the guanine base but not thymine, cytosine and adenine bases as estimated with the g value of 2.0150. On the other hand, the singlet oxygen-generating C60 formed 8-hydroxydeoxyguanosine (8-OH-dG) upon treatment with 2' deoxyguanosine and microsomes or linoleate. The formation of 8-OH-dG was highly elevated in the presence of microsomes and linoleate. The level of 8-OH-dG formed with and without the microsome fraction was 47 and 9.6 units, respectively, per 10(4) deoxyguanosine. It was considered that the mechanism is indirect action of singlet oxygen due to lipid peroxidation of linoleate that causes oxidative DNA damage.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed1994

Detection of nitro-azabenzo[a]pyrene derivatives in the semivolatile phase originating from airborne particulate matter, diesel and gasoline vehicles.

Mutagens in the semivolatile phase of airborne particulate matter, diesel and gasoline engine emissions were investigated using chemical and biological assays. The previously unknown mutagens, 1-(3-)nitro-6-azabenzo[a]pyrenes (1-N-6-ABP and 3-N-6-ABP) and 1-(3-)nitro-6-azabenzo[a]pyrene-N-oxides (1-N-6-ABPO and 3-N-6-ABPO), were detected in the semivolatile phase, which was adsorbed onto XAD-4 resin combined with a Teflon-coated fibre filter. Dichloromethane extracts of materials adsorbed onto XAD-4 resin were divided into acidic, neutral and basic by liquid-liquid separation. These chemicals in the basic fraction were the major mutagens in the semivolatile phase when they were bioassayed using Salmonella typhimurium TA98 in the absence of S9 mix; the mutagenicity of the basic fraction contributed at the rate of 42.9-68.8% of that of crude extracts for airborne, diesel and gasoline emission materials. As the mutagens were found to be difficult to analyse by gas chromatography (because of their probable absorption onto the packing) they were purified by HPLC and analysed by mass spectrometry. The concentrations of 1-N-6-ABP, 3-N-6-ABP, 1-N-6-ABPO and 3-N-6-ABPO detected were 1.1, 1.2, 0.8 and 0.3 ng/g, respectively, of materials in the airborne sample, and 4.9, 7.7, 2.2 and 3.8 ng/g, respectively, of materials in the diesel emission. Only 1-N-6-ABP (3.4 ng/g) and 3-N-6-ABP (4.9 ng/g) were detected in the semivolatile phase of the gasoline engine emission.(ABSTRACT TRUNCATED AT 250 WORDS)

Air Pollutants↗
PubMed1994

Mutagenic and carcinogenic significance and the possible induction of lung cancer by nitro aromatic hydrocarbons in particulate pollutants.

Studies of genotoxicity and carcinogenicity of nitro aromatic hydrocarbons focus on their high mutagenicity for bacteria and mammalian cells. Nitrobenzo[a]pyrenes (NBPs) and related nitroazaarenes also are extraordinarily mutagenic. 3-Nitro-6-azabenzo[a]pyren-N-oxide was found to be a more potent mutagen than 1,8-dinitropyrene. Mutagenicity of NBPs was associated with the position of substitution of the nitro function when nitrogen dioxide (NO2) was substituted at the third position on the benzo[a]pyrene (BP) structure, as in 3,6-dinitrobenzo[a]pyrene but not in 1,6-diNBP. The NBPs were reduced by a rat liver postmitochondrial fraction to nitroso- and subsequently to amino-derivatives. Therefore, tumoral action in rats was induced at significant levels by subcutaneous injection of 3,6-diNBP, but no tumors were observed in rats given 1,6-diNBP. Carcinogenic nitropyrenes were detected in the resected lung of a patient with lung cancer. It is suggested that the presence of nitropyrenes and the resulting tumor were due to exposure to by-products of combustion of heavy oil. The patient was a nonsmoker and farmer who had bred chickens for 40 years. He used heavy oil for heating the chicken house. Similarly, a group of Chinese people at high risk of developing lung cancer was selected to determine the initiator of lung cancer. Lung cancers were obtained from six Chinese female nonsmokers who were living in Fuyuan County, China. Polycyclic aromatic hydrocarbons were detected in resected lung specimens; they were benzo[k]fluoranthene, BP, benzo[g,h,i]perylene, and pyrene. These cases were associated with exposure to soot from combustion of coal usually used for heating and cooking indoors.

Adult↗
PubMed1993

Chromosomal aberrations induced in vitro by 3,7- and 3,9-dinitrofluoranthene.

The chromosomal aberration test using a Chinese hamster cell line (CHL) was carried out with 3,7- and 3,9-dinitrofluoranthene (DNF) with and without exogenous metabolic activation (rat liver S9 mix). The highest dose tested was limited to 20 micrograms/ml because of the compounds' insolubility in dimethyl sulfoxide. Both DNFs induced chromosomal aberrations in the absence of S9 mix; the frequency was not very high. Results were reproducible, but without clear dose-response relationships. Neither DNF induced chromosomal aberrations in the presence of S9 mix. Both DNFs did not induce polyploid cells under any conditions.

Aneuploidy↗
PubMed1993

The presence of mutagens/carcinogens in the excised lung and analysis of lung cancer induction.

To elucidate a relationship between lung cancer and tumor induction of environmental chemicals, the presence of 1-nitropyrene (1-NP) and benzo[a]pyrene (B[a]P) in 137 Japanese (97 male and 40 female), and 21 Chinese lung specimens was examined by HPLC, and GC-MS and environmental exposure discussed. Mortality due to lung cancer in Fuyuan County, China, is much higher than that of other cancers. We investigated 21 patients who were residents of Fuyuan County. All were female aged 28-64 years and were non-smoking farmers and cooks. The histological features of the tumors were adenocarcinoma, squamous cell carcinoma and small cell carcinoma. The incidence of cancer was due to inhaling soot from the combustion of coal used for cooking and indoor heating. The polycyclic aromatic hydrocarbons, chrysene, benzo[k]fluoranthene, B[a]P, benzo[g,h,i]perylene and pyrene, but not their nitrated derivatives, were detected in substantial amounts in the resected lungs. These mutagens and carcinogens normally originate in combustion products of coal, and are discussed as the possible initiators of the tumors in the lungs of these patients. All the Japanese lung specimens were also obtained from non-smokers. The concentrations of 1-NP averaged 21.3 +/- 12.4 and 5.9 +/- 2.4 pg/g of Japanese and Chinese samples respectively. The concentrations of B[a]P averaged 180.2 +/- 103.7 and 608.7 +/- 477.1 pg/g of Japanese and Chinese samples respectively. Thus, Japanese and Chinese lung specimens were mainly contaminated by 1-NP and B[a]P, respectively. Typical tissues from a carcinomatous human lung were examined. The patient was a 64-year-old Japanese male non-smoker and farmer who had raised chickens over a period of 40 years. The histological features of the tumor were those of keratinizing squamous cell carcinoma. 1-Nitropyrene, 1-nitro-3-hydroxypyrene, 1,3-dinitropyrene and chrysene were detected at concentrations of 0.11, 0.036, 0.095 and 0.16 ng respectively per gram of lung tissue. This cancer was due to long-term exposure to the combustion products of heavy oil used in a chicken house.

Adenocarcinoma↗
PubMed1992

Mutagenicity of nitro-azabenzo[a]pyrene and its related compounds.

The mutagenicity of nitrated benzo[a]pyrene (BP) and the related compounds, 1- and 3-nitrobenzo[a]pyrene (NBP), 1- and 3-nitro-6-cyanobenzo[a]pyrene (N-6-CBP), 1- and 3-nitro-6-azabenzo[a]-pyrene (N-6-ABP), 1- and 3-nitro-6-azabenzo[a]-pyrene-N-oxide (N-6-ABPO) and 1,6- and 3,6-dinitrobenzo[a]-pyrene (DNBP), was investigated. The mutagenic activities of 3-N-6-CBP and 3-N-6-ABP were 117 and 76 times, respectively, that of 3-NBP. In addition, 3,6-DNBP was more mutagenic than 1,6-DNBP. It is suggested that the mutagenic activation differs with the position of NO2 substitution in the chemical structure. A nitro derivative with NO2 substitution at the 3 position of the aromatic ring of BP was more mutagenic than that with the substitution at the 1 or 6 position. The reducibility of DNBPs was then determined by detecting 1- or 3-amino-6-nitrobenzo[a]pyrene (A-6-NBP), a metabolite of DNBP; 3,6- and 1,6-DNBP were reduced to 3- and 1-A-6-NBP at frequencies of 958 +/- 26 and 79 +/- 8, respectively, pmole per mg of protein, when the compound was incubated anaerobically with rat liver S9 mix at 37 degrees C for 15 min. NO2 substituted at the 3 position of the aromatic ring of BP was readily reduced by a microsome enzyme to form an amino derivative. The result suggests that these compounds have a structure-activity relationship between mutagenicity and NO2 substitution of BP.

Animals↗
PubMed1991

Detection of 3,6-dinitrobenzo[a]pyrene in airborne particulates.

3,6-Dinitrobenzo[a]pyrene, a new mutagen, was detected in airborne particulates collected in Santiago (Chile). The quantity of the compound in the airborne particulates was very small, accounting for 0.01 micrograms/g of total particulates (0.002 ng/m3 of air) at the lowest concentration. It was found that 3,6-dinitrobenzo[a]pyrene is readily decomposed by UV irradiation at 312 nm. The decomposed product was identified as 3-nitrobenzo[a]pyrene-6-quinone by means of mass spectrometry and proton nuclear magnetic resonance analysis. The mutagenicity of 3,6-dinitrobenzo[a]pyrene was 137,000 revertants/nmole for Salmonella typhimurium strain TA98, less than that for strain TA98/1,8-DNP6, an acetyltransferase-deficient mutant, and more than that for strain YG1024, an acetyltransferase-rich mutant.

Air Pollutants↗
PubMed1991

Pulmonary carcinogenicity of 3,9- and 3,7-dinitrofluoranthene, 3-nitrofluoranthene and benzo[a]pyrene in F344 rats.

3,9- and 3,7-Dinitrofluoranthene (3,9- and 3,7-DNF), 3-nitrofluoranthene (3-NF) and benzo[a]pyrene (B[a]P) were tested for pulmonary carcinogenicity by intrapulmonary implantation of the compounds into rat lung. These chemicals were given in various doses as suspensions in beeswax-trycaprylin and the animals were observed for 100 weeks. The control group received no drugs. The incidences of lung tumors were 19/21 (90.5%), 7/10 (70%) and 1/10 (10%) in rats treated with 200, 100 and 50 micrograms of 3,9-DNF, 4/9 (44.4%), 3/10 (30%) and 0/10 (0%) in rats treated with 200, 100 and 50 micrograms of B[a]P, 12/22 (54.5%) in rats treated with 200 micrograms of 3,7-DNF and 1/20 (5%) in rats treated with 1000 micrograms of 3-NF respectively. No lung tumors were found in control rats. The incidence of lung tumors induced by 3,9-DNF was twice as high as that induced by B[a]P, when the equivalent dose levels of the two compounds were compared. Histologically, most of the tumors induced by 3,9- and 3,7-DNF and B[a]P were squamous cell carcinomas.

Animals↗
PubMed1990

Induction of nitroarenes in cigarette smoke condensate treated with nitrate.

Samples of cigarette smoke condensates (CSCs) treated with nitric acid or Chinese cabbage pickles having a high nitrate content strongly mutated Salmonella typhimurium strain TA98; the benzene/ethanol extract after these treatments induced 1800 and 820 revertants, respectively, per mg of extract for strain TA98 in the absence of S9 mix. The major mutagens in these materials were found to be 1-nitropyrene and 1,3-dinitropyrene on the basis of the result of gas chromatography/mass spectrometry and of fluorescence spectra of the samples. The quantity of 1-nitropyrene was 14.5 ng per cigarette for the CSCs treated with nitric acid, and for 11.2 ng for those treated with Chinese cabbage pickles. Similarly, 1,3-dinitropyrene was detected in the CSCs treated with nitric acid or Chinese cabbage pickles at concentrations of 0.38 and approximately 0.1 ng, respectively, per cigarette.

Biotransformation↗
PubMed1989

Identification of mutagens in Japanese pickles.

A total of 108 samples of pickles, which were produced in districts with high and low incidences of stomach cancer in Japan, were extracted with methanol-chloroform. The extracts were bioassayed with Salmonella tester strains. The pickles produced in the high-cancer-incidence district were more mutagenic than those produced in the low-incidence district. The most mutagenic sample among 24 pickle specimens collected in the high-incidence district induced 130 revertants/mg of the crude extract for strain TA98. The mutagenic compounds were purified, and 2 flavonols, quercetin and rhamnetin, were identified as the major mutagens in the pickles by gas chromatography-mass spectrometry. The quantities of the 2 compounds were determined as 6.60 mg for quercetin, and 1.96 mg for rhamnetin per gram of the crude extract. The mutagenic activities of the pickles produced in the 2 districts were closely related to the amounts of quercetin in them.

Biotransformation↗
PubMed1987

Dinitrofluoranthene: induction, identification and gene mutation.

By renitrating 3-nitrofluoranthene in the presence of fuming nitric acid, some additional nitro-derivatives were induced; they were identified as 3,7-, 3,9- and 3,4-dinitrofluoranthene (DNF), and two trinitrofluoranthenes (TNF, 3,4,7- and 3,4,8- or 3,4,9-isomers) on the basis of the results of mass spectrometry and 1H-nuclear magnetic resonance. The yield of 3,7- and 3,9-DNF was about 61.3% in all of the derivatives induced. All of the DNFs yielded positive results in the rec-assay system, inducing DNA-damaging activity in Bacillus subtilis. Both 3,7- and 3,9-DNF converted Salmonella typhimurium His- strains TA98, TA97 and TA1538 from autotrophy to prototrophy, indicating a frameshift-type mutation for both; for strain TA98, 3,7-, 3,9- and 3,4-DNF gave mutagenicity of 422, 355 and 15.5 His+ revertants, respectively, per nanogram, corresponding to the specific activity of 1,6-dinitropyrene (DNP), a powerful mutagen. These DNFs are known to be potential mutagens which are eluted at adjacent retention times with 1,3-, 1,6- and 1,8-DNP on a column for high-performance liquid chromatography.

Bacillus subtilis↗
PubMed1987

Induction of subcutaneous tumors in rats by 3,7- and 3,9-dinitrofluoranthene.

Two dinitrofluoranthenes (DNFs) derived from 3-nitrofluoranthene were purified to over 99%, and tested for tumorigenicity in F344/DuCrj male rats. Rats were inoculated s.c. with 0.05 mg 3,7- or 3,9-DNF twice a week for 10 weeks. All 21 rats given 3,7-DNF and 10 of 11 rats (91%) given 3,9-DNF developed tumors at the injection site by 48 weeks after the first injection. Twenty of the 21 tumors induced by 3,7-DNF and seven of the 10 tumors induced by 3,9-DNF were classified as malignant fibrous histiocytoma, but one tumor in the 3,7-DNF-treated group and three tumors induced by 3,9-DNF showed typical features of rhabdomyosarcoma. The first tumors in 3,9-DNF-treated rats appeared on day 88 (on day average 117), 10 weeks earlier than in 3,7-DNF-treated ones (on day average 186).

Animals↗