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PubMed1976

The metabolic activation of the carcinogen 1'-hydroxysafrole in vivo and in vitro and the electrophilic reactivities of possible ultimate carcinogens.

Administration of [2',3'-3H]-1'-hydroxysafrole to rats or mice resulted in the formation of hepatic DNA-, ribosomal RNA-, and protein-bound 3H derivatives. Alkaline digestion of the 3H-protein released 0.1 to 0.3% of the 3H as a derivative that was identified as 3'-methylmercaptoisosafrole by its cochromatography in five solvent systems with the synthetic compound. 1'-Hydroxysafrole was metabolized at a low rate by rat and mouse liver cytosols in a 3'-phosphoadenosine 5'-phosphosulfate-dependent reaction to a derivative (presumably the sulfuric acid ester) that was captured by its reaction with RNA. Likewise, 1'-hydroxysafrole was oxidized at a low rate by rat and mouse liver microsomes to 1'-hydroxysafrole-2',3'-oxide in a reduced nicotinamide adenine dinucleotide phosphate-dependent reaction. Both of these electrophilic metabolites are candidate ultimate carcinogenic derivatives of 1'-hydroxysafrole. The electrophilic reactivities of various safrole derivatives with nucleosides were determined to be in the order of 1'-oxosafrole greater than 1'-acetoxysafrole greater than 1'-acetoxysafrole-2',3'-oxide greater than 1'-hydroxysafrole-2',3'-oxide greater than safrole-2',3'-oxide greater than or equal to 1'-oxosafrole-2',3'-oxide. The major reactions were generally observed with guanosine. A major reaction product of 1'-acetoxysafrole and guanosine 5'-monophosphate yielded 3'-hydroxyisosafrole under very mild acidic conditions. These data further substantiate the previous characterization of this reaction product as O-6-(isosafrol-3'-yl)guanylic acid. The syntheses of 1'-oxosafrole, 2',3'-dehydrosafrole, [2',3'-3H]-1'-hydroxysafrole, and the 2',3'-oxed.

Acetyltransferases↗
PubMed1984

Characterization of the biliary and urinary glutathione and N-acetylcysteine metabolites of the hepatic carcinogen 1'-hydroxysafrole and its 1'-oxo metabolite in rats and mice.

The hepatocarcinogen safrole is metabolized both to 1'-hydroxysafrole, a proximate hepatocarcinogen, and to 1'-oxosafrole, which is electrophilic but has little or no carcinogenic activity in rats and mice. As a part of a study on the metabolic interrelationships of these metabolites, their biliary and urinary conjugates were investigated. Administration of a single i.p. dose of [2',3'-3H]-1'-oxosafrole to male Sprague-Dawley rats or female CD-1 mice with cannulated bile ducts resulted in the excretion of 2 major biliary metabolites. These metabolites were isolated by high-performance liquid chromatography and characterized by 1H-nuclear magnetic resonance spectroscopy as 3'-(glutathion-S-yl)-1'-oxo-2',3'-dihydrosafrole and 3'-(N-acetylcystein-S-yl)-1'-oxo-2',3'-dihydrosafrole. The latter conjugate was also found in the urine. These conjugates were synthesized by non-enzymatic reaction of 1'-oxosafrole with glutathione and N-acetylcysteine at pH 8. After a single i.p. dose of [2',3'-3H]-1'-hydroxysafrole, the major biliary and urinary metabolite in rats was the glucuronide of this alcohol. Lower levels of the glutathione and N-acetylcysteine conjugates of 1'-oxosafrole appeared in the bile, and the latter conjugate was also found in the urine. Similar findings were made on the biliary metabolites of 1'-hydroxysafrole in mice. Although the sulfuric acid ester of 1'-hydroxysafrole is the major metabolite leading to the formation of DNA adducts in the liver, it was, at most, of minor importance in the formation of glutathione adducts. Only a very small percentage of a dose of 1'-hydroxysafrole was excreted in the bile of rats or mice as products that cochromatographed with 1'-(glutathion-S-yl)-safrole and 3'-(glutathion-S-yl)-isosafrole; no 3'-(N-acetylcystein-S-yl)-isosafrole was detected. These latter conjugates were synthesized by nonenzymatic reactions at pH 8.5 of the model electrophilic ester 1'-acetoxysafrole with glutathione or N-acetylcysteine.

Acetylcysteine↗
PubMed1996

Covalent binding to DNA in vitro of 2',3'-oxides derived from allylbenzene analogs.

Epoxidation at the allylic side chain is a major metabolic pathway for allylbenzene and its naturally occurring analogs safrole, estragole, and eugenol. We demonstrate herein that the epoxide metabolites of allylbenzene, estragole, and safrole can form covalent adducts with DNA in vitro, binding primarily to guanine, but also to the other three DNA bases. Epoxide hydrolases can prevent the binding of allylbenzene 2',3'-oxide to DNA in vitro. Four distinct adducts were detected by analytical TLC after the reaction of 2'-deoxyguanosine with allylbenzene 2',3'-oxide. One unstable adduct was formed rapidly, but gradually disappeared, whereas the other three adducts were formed more slowly but persisted. The major persistent adduct, which was isolated by preparative chromatography, was examined by MS and NMR. The structure of this adduct is 3'-N1-deoxyguanosyl-(2'-hydroxypropylbenzene). In addition, a generally applicable paradigm for the identification of deoxyguanosine or guanosine adducts by 13C and 1H NMR spectroscopy is presented.

Animals↗
PubMed1994

Further studies with the somatic white-ivory system of Drosophila melanogaster: genotoxicity testing of ten carcinogens.

To provide further background data for the white-ivory somatic mutation Drosophila assay, ten selected carcinogens (acetamide, acrylamide, benzo(alpha)pyrene, cyclophosphamide, diethylstilbestrol, 4-nitroquinoline N-oxide, propyleneimine, safrole, thiourea, and o-toluidine) have been tested in this system. Seventy-two hours after egg laying, larvae were fed with different concentrations of each carcinogen during the rest of their development until pupation, and the genotoxic effects were measured as significant increases in the appearance of visible mutant clones of ommatidia in the eyes of the emerging adult flies. Our results indicate that three of the ten carcinogens tested (cyclophosphamide, 4-nitroquinoline N-oxide, and propyleneimine) were strong genotoxic agents, two (diethylstilbestrol and acrylamide) induced significant positive results but without a dose-response relationship, and safrole was weakly positive. On the other hand, acetamide, benzo(alpha)pyrene, thiourea, and o-toluidine were unable to increase the frequency of mutant clones.

Animals↗
PubMed1987

Immunohistochemical demonstration of decreased L-pyruvate kinase in enzyme altered rat liver lesions produced by different carcinogens.

Preneoplastic liver lesions were produced in female Wistar rats by application of 25 mg/kg N-nitrosomorpholine (NNM), 14 mg/kg diethylnitrosamine (DENA), 0.075 mg/kg aflatoxin B1 (AFB1) or 160 mg/kg safrole. These carcinogens were administered in two equal doses 12 and 24 h after partial hepatectomy. The animals then received sodium phenobarbital (0.1% in tap water) for up to 410 days. Numerous altered hepatic foci (AHF) and hyperplastic nodules (HN) were detected enzyme histochemically by their negative ATPase reaction after application of AFB1, DENA and NNM; some AHF and HN were also caused by the weak carcinogen safrole. Immunohistochemically these lesions were also L-pyruvate kinase (L-PK)-negative with a high coincidence with regard to their number and area. These results confirm the role of L-PK, an enzyme affecting the pentose phosphate pathway, as a negative marker of preneoplastic liver lesions.

Animals↗
PubMed1993

The in vitro micronucleus test on isolated human lymphocytes.

The in vitro micronucleus test was performed on isolated human lymphocytes using the cytokinesis-block technique with and without a rat liver metabolizing system. Positive control substances were used to evaluate this test: a direct agent (vincristine) requiring no metabolic activation, and three promutagens (cyclophosphamide, benzo[a]pyrene and dimethylbenz[a]anthracene). All of them, when compared with controls, caused a significant increase in micronucleus frequency, with a clear dose response. Five compounds were then tested in this in vitro micronucleus test: safrole, azathioprine, procarbazine, diethylstilbestrol and o-toluidine. The chemicals were examined with and without exogenous metabolic activation. Of these five compound, o-toluidine was found to be a marked direct genotoxic agent and azathioprine gave positive results with or without metabolic activation (a better response was noted without the addition of S9 mix). Diethylstilbestrol gave conflicting results and was considered inconclusive. Two chemicals, safrole and procarbazine, were found to be non-genotoxic in this test system, whatever the protocol used.

Adult↗
PubMed1990

Structure-specificity of the genotoxicity of some naturally occurring alkenylbenzenes determined by the unscheduled DNA synthesis assay in rat hepatocytes.

A number of alkenylbenzenes related to safrole and estragole are known to be hepatocarcinogenic in rats and/or mice, apparently by a genotoxic mechanism. However, they are not bacterial mutagens in the Ames test. We have studied the ability of a series of carcinogenic and non-carcinogenic congeners to induce unscheduled DNA synthesis (UDS) in freshly isolated rat hepatocytes in primary culture. The cytotoxicity of these compounds was assessed by lactate dehydrogenase leakage. There was an excellent correlation between UDS induction and known rodent hepatocarcinogenicity, with safrole, estragole and methyleugenol all inducing UDS. Anethole, isosafrole, eugenol and allylbenzene, for which evidence of carcinogenicity is equivocal or negative, did not induce UDS. All compounds were markedly cytotoxic at concentrations between 10(-3) and 10(-2) M, irrespective of their structural features. The data are discussed with reference to the known structure dependence of the disposition of the alkenylbenzenes, notably their metabolic activation, with which there are excellent correlations. The demonstration of the genotoxicity of rodent hepatocarcinogenic alkenylbenzenes in cells cultured from the in vivo target organ will allow the direct investigation of factors influencing these processes and facilitate the safety evaluation of these important natural flavours.

Animals↗
PubMed1983

Psychopharmacological effects of the essential oil fraction and of the hydrolate obtained from the seeds of Licaria puchury-major.

An essential oil fraction obtained from powdered seeds of Licaria puchury-major contained 51.3% of safrol, 3.3% of eugenol and 2.9% of methyleugenol, among other substances. Fifty to 800 mg/kg of this fraction reduced motor activity and anesthetized mice; it also protected the animals against transcorneal electroshock. A hydrolate obtained from the powder, contained 0.2 mg of essential oil fraction per ml: 0.1 and 0.2 ml/10 g of this hydrolate reduced motor activity and potentiated barbiturate sleeping time of mice; 2.5-10 ml/kg given to rats produced a drop in body temperature. The hydrolate, however, did not anesthetize and did not protect mice against convulsions induced by electrical shock. These amounts of the hydrolate corresponded to dosing the animals with 2-4 mg/kg of the essential oil (or 1-2 mg/kg of safrol), doses which were inactive per se. This suggested that the pharmacological activity of the hydrolate was not due to its essential oil content. Corroborating this possibility the hydrosoluble portion of the hydrolate mimicked all of its effects: reduced motor activity, potentiated barbiturate sleeping time of mice and decreased body temperature of rats. The hydrosoluble material, as the hydrolate, was also incapable of anesthetizing and protecting mice against electroshock induced convulsions.

Animals↗
PubMed2005

Determination of synthesis method of ecstasy based on the basic impurities.

MDMA was prepared by five different synthesis routes, i.e. by dissolving metal reduction (Al/Hg), cyanoborohydride reduction (NaBH(3)CN), borohydride reduction in low temperature (NaBH(4)), Leuckart reaction and safrole bromination. MDP-2-P was prepared by two different synthesis methods, i.e. by isosafrole oxidation and MDP-2-nitropropene reduction. Each of the synthesis routes was repeated three times in order to establish variation in qualitative composition of route specific impurities between different batches. The analysis of impurities in MDP-2-nitropropene, MDP-2-P, bromosafrole and MDMA was performed with GC-MS. GC/MS was used also in the analysis of impurities in starting materials: safrole, isosafrole and piperonal. As a result of our study the way of determination of MDMA synthesis route determination based on qualitative composition of impurities is proposed.

Journal Article↗
PubMed2001

Investigation of the role of the 2',3'-epoxidation pathway in the bioactivation and genotoxicity of dietary allylbenzene analogs.

The genotoxic potential of naturally occurring allylbenzene analogs, including safrole, eugenol, estragole, and others, has been examined in many studies over the past 30 years. It has been established that these compounds are subject to biotransformation in the liver, which can lead to the formation of reactive electrophilic intermediates. The major route of bioactivation is via hydroxylation of the 1' carbon atom of the allylic side chain. We have synthesized 2',3'- (allylic) epoxide derivatives of allylbenzene, estragole eugenol and safrole, and have used them to characterize the genotoxic potential of epoxidation at the allylic double bond for allylbenzene and its naturally occurring analogs. In order to assert that this pathway has the potential for genotoxicity, it is necessary to demonstrate (1) that epoxide metabolites of these compounds are capable of forming covalent adducts with DNA bases; and (2) that these epoxide metabolites are actually formed in vivo. We have demonstrated that allylic epoxides derived from allylbenzene and estragole are capable of forming covalent adducts with all four deoxyribonucleotides in vitro and, in the case of deoxyguanosine, form at least four different adducts. We also deduce, from evidence obtained using the isolated perfused rat liver, that formation of potentially genotoxic 2',3' epoxide metabolites occurs readily in vivo, but that these metabolites are rapidly further metabolized to less toxic dihydrodiol or glutathione conjugates. We conclude that 2',3' epoxide metabolites of allylbenzene analogs are formed in vivo and that these epoxides are sufficiently reactive to facilely form covalent bonds with DNA bases. Epoxide formation at the allylic double bond represents, therefore, a potentially genotoxic bioactivation pathway for allylbenzene analogs. However, comparison of the relative kinetics of epoxide metabolism and epoxide formation suggests that a wide margin of protection from DNA covalent adduct formation exists in the rat liver, thus preventing genotoxicity resulting from this pathway to any significant degree. In this regard, we have also observed that the general rate of epoxide hydrolysis is much greater in human liver than in rat liver. We therefore suggest that while the epoxidation pathway poses a potential genotoxic threat to humans, no actual genotoxicity occurs as a result of this metabolic pathway.

Animals↗
PubMed2000

Evaluation of the single cell gel electrophoresis assay with human hepatoma (Hep G2) cells.

Human Hep G2 cells have retained the activities of phase I and phase II enzymes which are involved in the metabolism of environmental genotoxins. The present study describes the results of single cell gel electrophoresis (SCGE) assays with a panel of different model compounds with these cells. With genotoxic carcinogens such as aflatoxin B(1) (AFB(1)), benzo(a)pyrene (B(a)P), nitrosodimethylamine (NDMA) and cyclophosphamide (CP), statistically significant dose dependent induction of DNA migration was measured. With the two heterocyclic amines, 2-amino-3-methyl-3H-imidazo[4, 5-f]quinoline (IQ) and 3-amino-1,4-dimethyl-5H-pyrido[4,3-b]indole (Trp-P-1), and also with rodent carcinogens such as safrole, hexamethylphosphoramide (HMPA) and the pyrrolizidine alkaloid isatidine, which give negative results in other in vitro genotoxicity tests, positive results were obtained in Hep G2/SCGE assays. Nitrosomethylurea (NMU) was the only directly acting compound tested in the study and was by far (ca. 10(3)-fold) more active than the corresponding nitrosamine. The exposure concentrations required to cause significant effects varied over a broad range. The most pronounced effect was seen with AFB(1) (0.008 microM) followed by HMPA (15 microM), B(a)P (25 microM), NMU (100 microM), isatidin (500 microM), CP (900 microM), IQ (1200 microM), safrol (4000 microM), and NDMA (90x10(3) microM). Numbers in parenthesis give the lowest concentrations, which caused a significant increase of DNA migration. With two compounds, namely, the non-carcinogen pyrene and the synthetic hormone tamoxifen (TF), negative results were obtained under all test conditions. These findings are in agreement with the results of recent investigations which indicated that human hepatocytes are unable to convert TF to DNA reactive metabolites, whereas it is activated by rat liver cells and causes DNA adducts in these cells. Comparisons of the present results with data from earlier experiments indicate that the Hep G2/SCGE assay enables the detection of genotoxins including compounds which give misleading results in other in vitro genotoxicity tests and appears to be an alternative to tests with primary liver cells from laboratory animals.

Biotransformation↗
PubMed1995

Salmonella test positive and negative carcinogens show different effects on intrachromosomal recombination in G2 cell cycle arrested yeast cells.

There is considerable controversy about the extrapolation of results obtained with high doses of chemicals in long-term and animal carcinogenesis studies to the low doses human beings are exposed to. In the present study, we compare the effect of Salmonella test positive carcinogens, ethyl methanesulfonate, methyl methanesulfonate, 4-nitroquinoline-1-oxide and gamma-rays versus Salmonella test negative carcinogens, benzene, safrole, urethane, thiourea and carbon tetrachloride over a dose range of 10(4)-fold on the frequency of intrachromosomal recombination in Saccharomyces cerevisiae. This short-term test is positive with both kinds of carcinogens. The Salmonella test negative carcinogens safrole, benzene and carbon tetrachloride induced intrachromosomal recombination to much higher levels in G2 arrested cells compared to growing cells; the reverse was true for the Salmonella test positive carcinogens. The Salmonella test positive carcinogens caused an almost linear dose response for induction of intrachromosomal recombination starting at a dose 100- to 1000-fold below the lowest toxic dose. In contrast, all Salmonella test negative carcinogens showed a sharp threshold below which no effect was detected, and the first effective dose for induction of intrachromosomal recombination was the first toxic dose.

Animals↗
PubMed1988

The initiator tRNA acceptance assay as a short-term test for carcinogens. 2. Results with ten compounds selected by the International Programme on Chemical Safety for the evaluation of short-term tests for carcinogens.

Eight carcinogenic and two non-carcinogenic compounds that are difficult to detect by short-term tests (acrylonitrile, benzene, benzoin, caprolactam, diethylhexylphtalate, diethylstilbestrol, hexamethylphosphoramide, phenobarbital, safrole and o-toluidine) were tested independently in Prague and in Heidelberg by the newly developed initiator tRNA acceptance assay. Seven out of eight tested carcinogens gave a positive response in this assay, only safrole showed a false negativity in both laboratories. Both non-carcinogenic compounds, benzoin and caprolactam, exhibited no activity. An absolute qualitative agreement was found with all compounds tested between the results of both laboratories. With the exception only of phenobarbital (intermediate activity in Prague and low in Heidelberg) the quantitative results obtained in both laboratories were comparable. The initiator tRNA acceptance assay thus appears to be a reliable short-term test for carcinogenicity with good reproducibility.

Carcinogens↗
PubMed1984

Carcinogen induced unscheduled DNA synthesis in mouse hepatocytes.

Mouse primary liver cell cultures were examined for evidence of unscheduled DNA synthesis (UDS) following treatment with the carcinogens; dimethylnitrosamine (DMNA), diethylnitrosamine (DENA), 2-acetylaminofluorene (2-AAF), N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), benzo(a)pyrene (BP), dimethylbenzanthracene (DMBA), 1,1,-bis(p-chlorophenyl)-2,2,2-trichloroethane (DDT), safrole, diethylstilbestrol (DES), aflatoxin B1 (AFB1), and dieldrin and the noncarcinogens; dimethylformamide (DMF), fluorene, and pyrene. Mouse hepatocyte cultures were simultaneously treated with three concentrations of each compound and 3H-thymidine. After 24 hrs, cells were fixed and processed for autoradiography. 3H-thymidine incorporation in both experimental and control cell nuclei, as evidenced by autoradiographic grains, was quantitated microscopically. DMNA, DENA, 2-AAF, MNNG, BP, AFB1 and DMBA significantly increased UDS over untreated cells at all concentrations studied. DDT, DMF, fluorene, pyrene, safrole, DES, and dieldrin were negative for UDS in all concentrations examined. DMNA, 2-AAF and MNNG were also studied for UDS induction in 2 hr old, 1 day old and 4 day old cultures. A progressive decrease in UDS with increased time after plating was found in DMNA and 2-AAF treated cultures. After 4 days DMNA and 2-AAF induced UDS only at the highest concentrations examined (10(-3) M and 10(-4) M respectively). MNNG induced UDS at all time periods and concentrations sampled. An attempt to enhance the sensitivity of the UDS assay by inducing the mixed function oxidative enzyme activity in the hepatocytes with phenobarbital administered in vivo resulted in no statistically significant increase in UDS with DMNA, 2-AAF, MNNG, DDT, and dieldrin when compared with cells from non-induced animals.

Animals↗
PubMedDate not supplied

Micronucleus formation in human lymphocytes and in the metabolically competent human hepatoma cell line Hep-G2: results with 15 naturally occurring substances.

To examine the concordance of two metabolizing systems for use in genotoxocity testing with the micronucleus test, 15 naturally occurring substances (arecoline, the plant extract aristolochic acid, beta-asarone, benzyl acetate, coumarin, emodine, isatidine dihydrate, monocrotaline, psoralen, reserpine, retrorsine, safrole, sanguinarine chloride, tannin and thiourea) were tested for their genotoxicity in the cytokinesis-block micronucleus test in vitro with human lymphocytes and in the presence and the absence of an exogenous metabolizing system from rat liver S9-mix and the metabolically competent human hepatoma cell line Hep-G2. Arecoline, the plant extract aristolochic acid, psoralen and tannin caused a significant increase in the number of micronuclei in human lymphocytes in the presence and the absence of an exogenous metabolising system from rat liver S9-mix and the metabolically competent human hepatoma cell line Hep-G2. A significant increase in the number of micronuclei with beta-asarone, coumarin, monocrotaline and retrorsine could be detected in the presence of S9-mix and the cell line Hep-G2. Benzyl acetate, emodine, isatidine dihydrate, reserpine, safrole, sanguinarine chloride and thiourea did not reveal any micronucleus inducing activity in either human lymphocytes or in Hep-G2. In addition to the other Hep-G2 results in the literature, this human hepatoma cell line could have a useful potential in the in vitro micronucleus test.

Adult↗
PubMed2002

[Analysis of volatile constituents of root and rhizome of Asarum heterotropoides Fr. var. mandshuricum (Maxim.) Kitag. by gas chromatography-mass spectrometry].

The volatiles of root and rhizome of Asarum heterotropoides Fr. var. mandshuricum (Maxzim. ) Kitag. were extracted with n-hexane and analyzed by capillary gas chromatography-flame ionization detection and gas chromatography-mass spectrometry (GC-MS) with the same column HP-5 (30 m x 0.25 mm i.d.). Initial oven temperature was kept at 40 degrees C for 2 min, then raised to 160 degrees C at 3 degrees C /min, immediately raised to 250 degrees C at 6 degrees C /min, and kept 250 degrees C for 23 min. According to GC-MS analysis, 36 compounds were identified. The main components are safrole, methyleugenol, 3,5-dimethoxytoluene, pentadecane, N-isobutyldodecatetraenamide. Furthermore, the analysis results of root and rhizome were compared. The results indicate that the fundamental constituents are nearly the same, but the quantities of volatiles in root are richer than those in rhizome. In addition, 8 compounds are selected as the criteria of quality control, including 3-carene, 1,8-cineole, eucarvone, methyleugenol, safrole, myristicin, pentadecane and N-isobutyldodecatetraenamide.

Asarum↗
PubMed1993

32P-postlabelling analysis of small aromatic and of bulky non-aromatic DNA adducts.

The 32P-postlabelling methodology for analysis of DNA adducts derived from carcinogens containing one aromatic ring (e.g., safrole, styrene oxide, benzene metabolites, 1-nitrosoindole-3-acetonitrile) or a bulky non-aromatic moiety (e.g., mitomycin C, diaziquone) is reviewed. Six steps are involved: digestion of DNA to 3'-nucleotides, enrichment of adducts, 32P-labelling of adducts, separation of labelled adducts by TLC, detection, and quantitation. The first step, DNA digestion with micrococcal nuclease and spleen phosphodiesterase, is applicable to DNA modified with most carcinogens independent of their size and structure. Of the two commonly used procedures for enrichment of aromatic adducts in DNA digests, the nuclease P1 treatment is substantially more effective than butanol extraction for small aromatic and bulky non-aromatic adducts. For initial purification of these adducts from unadducted material after 32P-labelling, multi-directional polyethyleneimine (PEI)-cellulose TLC using 1 M sodium phosphate, pH 6.0, as the D1 solvent is not suitable, because they are not retained on PEI-cellulose under these conditions. A higher concentration of sodium phosphate (e.g., 2.3 M) or development with D1 and D3 solvents in the same direction helps to retain adducts of safrole and of benzene metabolites. Also, transfer of adducts from multiple cut-outs above the origin after D1 chromatography, as adopted for analysis of I-compounds, is potentially applicable. However, initial purification by reverse-phase TLC, followed by in situ transfer and resolution by PEI-cellulose TLC has been found to be most effective for these adducts. Reverse-phase TLC at 4 degrees C or in a stronger salt solution further improves retention of some adducts (e.g., mitomycin C and diaziquone adducts). For adduct separation by PEI-cellulose TLC, salt solutions with or without urea are used.

Carcinogens↗
PubMed1991

Genotoxicity studies with the unstable zeste-white (UZ) system of Drosophila melanogaster: results with ten carcinogenic compounds.

To increase the number of chemicals tested using the zeste-white (UZ) somatic mutation assay, ten selected carcinogens (acetamide, acrylamide, benzo(alpha)pyrene, cyclophosphamide, diethylstilbestrol, 4-nitroquinoline N-oxide, propyleneimine, safrole, thiourea, and o-toluidine) have been evaluated in this assay. Our results show that all the compounds tested produce significant increases in the eye spot frequency at, at least, one of the concentrations assayed, indicating that the zeste-white assay appears to be highly sensitive to these carcinogenic compounds. That is in agreement with data previously reported by other authors.

4-Nitroquinoline-1-oxide↗