Acetoxyacetylaminofluorene: An alkylating agent that forms DNA ADDUCTS at the C-8 position in GUANINE, resulting in single strand breaks. It has demonstrated carcinogenic action.Encyclopedias as Topic: Works containing information articles on subjects in every field of knowledge, usually arranged in alphabetical order, or a similar work limited to a special field or subject. (From The ALA Glossary of Library and Information Science, 1983)Copyright: It is a form of protection provided by law. In the United States this protection is granted to authors of original works of authorship, including literary, dramatic, musical, artistic, and certain other intellectual works. This protection is available to both published and unpublished works. (from Circular of the United States Copyright Office, 6/30/2008)Organizations, Nonprofit: Organizations which are not operated for a profit and may be supported by endowments or private contributions.Patents as Topic: Exclusive legal rights or privileges applied to inventions, plants, etc.MedlinePlus: NATIONAL LIBRARY OF MEDICINE service for health professionals and consumers. It links extensive information from the National Institutes of Health and other reviewed sources of information on specific diseases and conditions.Computer Security: Protective measures against unauthorized access to or interference with computer operating systems, telecommunications, or data structures, especially the modification, deletion, destruction, or release of data in computers. It includes methods of forestalling interference by computer viruses or so-called computer hackers aiming to compromise stored data.Confidentiality: The privacy of information and its protection against unauthorized disclosure.Molecular Biology: A discipline concerned with studying biological phenomena in terms of the chemical and physical interactions of molecules.Genetic Therapy: Techniques and strategies which include the use of coding sequences and other conventional or radical means to transform or modify cells for the purpose of treating or reversing disease conditions.Access to Information: Individual's rights to obtain and use information collected or generated by others.Genetic Vectors: DNA molecules capable of autonomous replication within a host cell and into which other DNA sequences can be inserted and thus amplified. Many are derived from PLASMIDS; BACTERIOPHAGES; or VIRUSES. They are used for transporting foreign genes into recipient cells. Genetic vectors possess a functional replicator site and contain GENETIC MARKERS to facilitate their selective recognition.Periodicals as Topic: A publication issued at stated, more or less regular, intervals.Biology: One of the BIOLOGICAL SCIENCE DISCIPLINES concerned with the origin, structure, development, growth, function, genetics, and reproduction of animals, plants, and microorganisms.Gene Transfer Techniques: The introduction of functional (usually cloned) GENES into cells. A variety of techniques and naturally occurring processes are used for the gene transfer such as cell hybridization, LIPOSOMES or microcell-mediated gene transfer, ELECTROPORATION, chromosome-mediated gene transfer, TRANSFECTION, and GENETIC TRANSDUCTION. Gene transfer may result in genetically transformed cells and individual organisms.Physicians: Individuals licensed to practice medicine.Internet: A loose confederation of computer communication networks around the world. The networks that make up the Internet are connected through several backbone networks. The Internet grew out of the US Government ARPAnet project and was designed to facilitate information exchange.Lawyers: Persons whose profession is to give legal advice and assistance to clients and represent them in legal matters. (American Heritage Dictionary, 3d ed)Child Advocacy: Promotion and protection of the rights of children; frequently through a legal process.Questionnaires: Predetermined sets of questions used to collect data - clinical data, social status, occupational group, etc. The term is often applied to a self-completed survey instrument.Attitude of Health Personnel: Attitudes of personnel toward their patients, other professionals, toward the medical care system, etc.Bites, Human: Bites inflicted by humans.

Cytosine methylation in a CpG sequence leads to enhanced reactivity with Benzo[a]pyrene diol epoxide that correlates with a conformational change. (1/93)

Benzo[a]pyrene (B[a]P) is a widespread environmental carcinogen that must be activated by cellular metabolism to a diol epoxide form (BPDE) before it reacts with DNA. It has recently been shown that BPDE preferentially modifies the guanine in methylated 5'-CpG-3' sequences in the human p53 gene, providing one explanation for why these sites are mutational hot spots. Using purified duplex oligonucleotides containing identical methylated and unmethylated CpG sequences, we show here that BPDE preferentially modified the guanine in hemimethylated or fully methylated CpG sequences, producing between 3- and 8-fold more modification at this site. Analysis of this reaction using shorter duplex oligonucleotides indicated that it was the level of the (+)-trans isomer that was specifically increased. To determine if there were conformational differences between the methylated and unmethylated B[a]P-modified DNA sequences that may be responsible for this enhanced reactivity, a native polyacrylamide gel electrophoresis analysis was carried out using DNA containing isomerically pure B[a]P-DNA adducts. These experiments showed that each adduct resulted in an altered gel mobility in duplex DNA but that only the presence of a (+)-trans isomer and a methylated C 5' to the adduct resulted in a significant gel mobility shift compared with the unmethylated case.  (+info)

Damaged DNA-binding proteins: recognition of N-acetoxy-acetylaminofluorene-induced DNA adducts. (2/93)

Proteins which bind to the DNA damaged by genotoxic agents can be detected in all living organisms. Damage-recognition proteins are thought to be generally involved in DNA repair mechanisms. On the other hand, the relevance to DNA repair of some other proteins which show elevated affinity to damaged DNA (e.g. HMG-box containing proteins or histone H1) has not been established. Using the electrophoretic mobility-shift assay we have investigated damage-recognition proteins in nuclei from rat hepatocytes. We detected two different protein complexes which preferentially bound the DNA damaged by N-acetoxy-acetylaminofluorene. One of them also recognized the DNA damaged by benzo(a)pyrene diol epoxide (yet with much lower efficiency). The proteins which bind to damaged DNA are permanently present in rat cells and their level does not change after treatment of animals with the carcinogens. Differences in the affinity of the detected damage-recognition proteins to DNA lesion evoked by either carcinogen did not correlate with more efficient removal from hepatic DNA of 2-acetylaminofluorene-induced adducts than benzo(a)pyrene-induced ones.  (+info)

DNA-damaging effects of genotoxins in mixture: nonadditive effects of aflatoxin B1 and N-acetylaminofluorene on their mutagenicity in Salmonella typhimurium. (3/93)

Most animal genotoxicity studies have used exposures to single chemicals; humans, however, are potentially exposed to mixtures of genotoxins. Cancer and developmental toxicity risks associated with genotoxins in mixture are generally estimated by assuming additivity of the components. Two or more genotoxins acting sequentially or simultaneously may present a greater or lesser hazard than that predicted by simple addition of their potencies. Previously, we studied the effect of one genotoxin on the binding of a second genotoxin to DNA in an in vitro system and demonstrated that consecutive binding of the two toxins was not additive. In the present study, the effect of one genotoxin on the mutagenicity of another was evaluated for two well-known genotoxins using the Salmonella assay. Pretreatment of frameshift strains TA98 and TA1538 with AFB1-8,9-epoxide (17.3 ng/plate) enhanced the mutagenicity induced by subsequent exposure to N-acetoxy-acetylaminofluorene (N-AcO-AAF) approximately 2-3 times above theoretical values for additivity. Pretreatment of base-substitution strain TA100 with N-AcO-AAF (0.1 microg/plate) inhibited the mutagenicity following subsequent exposure to AFB1-8,9-epoxide by 3 times below the theoretical additive value. Concentration-response relationships for these enhancing or inhibitory effects were demonstrated using increasing concentrations of the first genotoxin during pretreatment. These results demonstrate effects, other than additive, of sequential exposures to two genotoxins on the induction of mutations in a bacterial system.  (+info)

Synthesis of nuclear proteins during DNA repair synthesis in human diploid fibroblasts damaged with ultraviolet radiation of N-acetoxy-2-acetylaminofluroene. (4/93)

We have examined the accumulation of newly synthesized nuclear proteins into nuclei during DNA repair synthesis in confluent WI-38 human diploid fibroblasts damaged with ultraviolet radiation or N-acetoxy-2-acetylaminofluroene. In contrast to a marked stimulation of DNA repair synthesis, stimulation of amino acid incorporation into histone polypeptides or into the various molecular weight classes of nonhistone nuclear proteins was not observed. These results suggest that detectable stimulation of newly synthesized nuclear protein incorporation into nuclei does not accompany DNA repair synthesis induced by ultraviolet radiation or a direct acting chemical carcinogen. At least for the special case of repair, DNA synthesis may be uncoupled from histone synthesis.  (+info)

Enhancement of postreplication repair in Chinese hamster cells. (5/93)

Alkaline sedimentation profiles of pulse-labeled DNA from Chinese hamster cells showed that DNA from cells treated with N-acetoxy-acetylaminofluorene or ultraviolet radiation was made in segments smaller than those from untreated cells. Cells treated with a small dose (2.5 muM) of N-acetoxy-acetylaminofluorene or (2.5 J-m-2) 254-nm radiation, several hours before a larger dose (7-10 muM) of N-acetoxy-acetylaminofluorene or 5.0 J.m-2 of 254 nm radiation, also synthesized small DNA after the second dose. However, the rate at which this small DNA was joined together into parental size was appreciably greater than in absence of the small dose. This enhancement of postreplication repair (as a result of the initial small dose) was not observed when cells were incubated with cycloheximide between the two treatments. The results suggest that N-acetoxy-acetylaminofluorene and ultraviolet-damaged DNA from Chinese hamster cells are repaired by similar postreplicative mechanisms that require de novo protein synthesis for enhancement.  (+info)

DNA-protein cross-linking by chemical carcinogens in mammalian cells. (6/93)

The induction of DNA cross-linking in mammalian cells by various carcinogens was investigated by the method of alkaline elution. A dose-dependent increase in DNA cross-linking was seen following exposure of human fibroblasts to N-acetyoxy-2-acetylaminofluorene and following exposure of mouse embryo cells to 7,12-dimethylbenz[a]-anthracene. No cross-link effect was seen following treatment with N-methyl-N'-nitro-N-nitrosoguanidine, benz-[a]anthracene, benz[A]anthracene-5,6-dihydroepoxide, or metabolic inhibitors. The cross-linking appeared to be DNA-protein in nature since proteinase treatment removed the effect. DNA single-strand breaks were also induced by several of these agents in the case of N-acetoxy-2-acetylaminofluorene and N-methyl-N'-nitro-N-nitrosoguanidine, approximately 70 to 90% of these breaks were rejoined after an 18-hr incubation in fresh medium, whereas repair of the cross-links induced by N-acetoxy-2-acetylaminofluorene was slight at this time.  (+info)

Diverse chemical carcinogens fail to induce G(1) arrest in MCF-7 cells. (7/93)

The effect of three reactive potent chemical carcinogens on the passage of MCF-7 cells through the cell cycle was investigated. While these cells, which express wild-type p53, were arrested in G(1) after treatment with actinomycin D (a positive control), treatment with anti-benzo[a]pyrene dihydrodiol epoxide, N-acetoxy-N-2-fluorenylacetamide or N-methyl-N'-nitro-N-nitrosoguanidine, at doses consistent with survival of significant numbers of cells, caused the cells to accumulate in S phase, with little increase in those in G(1). This property of these three reactive potent carcinogens, of diverse chemical types, to induce evasion of G(1) arrest (the stealth property) presumably increases the likelihood of malignant change, because DNA replication continues on a damaged template. This stealth characteristic may be a major contributor to the tumorigenicity of DNA-adducting chemical carcinogens in general.  (+info)

Overlapping pathways for repair of damage from ultraviolet light and chemical carcinogens in human fibroblasts. (8/93)

DNA excision repair was measured in cultured human fibroblasts after single or dual treatments with ultraviolet radiation, 4-nitroquinoline 1-oxide, or N-acetoxy-2-acetylaminofluorene. Three approaches were used to monitor repair: unscheduled DNA synthesis, measured by autoradiography; repair replication, measured by the incorporation of a density-labeled DNA precursor into repaired regions; and excision of ultraviolet endonuclease-sensitive sites. When a single repair- saturating dose of one of the three carcinogens was administered, little stimulation of unscheduled DNA synthesis or repair replication could be observed by additional treatment with one of the other carcinogens. In no instance was total additivity of repair observed. These observations were confirmed by showing that the excision of endonuclease-sensitive sites produced by ultraviolet damage (i.e., pyrimidine dimers) was inhibited by exposure to 4-nitroquinoline 1-oxide and N-acetoxy-2-acetylaminofluorene. The data indicate that the repair of lesions induced by these substances may have common rate-limiting steps, a conclusion previously indicated by the repair deficiency in xeroderma pigmentosum cells in which a single mutation eliminates the repair of damage caused by each of these agents.  (+info)

Restriction enzyme inhibition and lambda exonuclease studies indicate that carcinogen N-acetoxy-N-acetyl-2 aminofluorene (AAAF) binds to sequences on ɸX174 RF and SV40 plasmids DNA that are similar to the eight preferred binding sites previously located on pBR 322. Both DNAs were digested with enzyme Hinf I and resultant fragments 32P end-labeled. Labeled fragments were reacted with the carcinogen to give one to sixteen bound moieties per DNA. Fragments were isolated and restriccion enzyme and lambda exonuclease inhibition assays were performed. Inhibition detected occurred at selected sites and was not specific for a certain enzyme or certain size of recognition sequence. Results of these assays allow mapping of the location of high affinity binding sites of the carcinogen on both DNAs. All sites have common sequence elements: the presence of either the sequence T(G/C)TT(G/C) or the sequence T(G/C) CTT(G/C).
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The mononuclear leukocytes from peripheral blood samples of individuals with (n = 30) and without (n = 48) colonic polyps were examined for their abilities to carry out unscheduled DNA synthesis (UDS) induced by N-acetoxy-N-2-fluorenylacetamide (N-AcO-2-FAA). Individuals with polyps had significantly reduced UDS values compared to the nonpolyp group (P , 0.01). Furthermore, in a more comprehensive study, patients with hyperplastic polyps had N-AcO-2-FAA-induced UDS values not significantly different from control individuals who were asymptomatic and free from colonic disease as judged by complete colonoscopy. However, patients who had had adenomatous polyps in their large bowel had significantly reduced levels of N-AcO-2-FAA-induced UDS in their mononuclear leukocytes (P , 0.005). When N-AcO-2-FAA binding to DNA determinations were made in parallel and DNA repair proficiency indices were calculated (i.e., N-AcO-2-FAA-induced UDS/N-AcO-2-FAA binding to DNA), the patients with adenomatous polyps ...
James joined AAAF in 2012 as a Support Ambassador after organising a charity cycle to raise awareness for Alopecia Areata. James became our ACT Branch Manager…
The AAAF blog, Love, Alopecia, is running a competition as part of our campaign for #HealthyAlopecia. To enter, write a story or article that fits the theme of…
Sorof, S and Dickens, M S., "Evidence for similar principal target proteins of chemical carcinogens in six carcinogen-organ systems. Abstr." (1978). Subject Strain Bibliography 1978. 443 ...
Like many non profit organisations, we struggled with finding the time to plan and execute on fundraising events. Tara hosted a fundraising event around cutting and donating her hair to campaign our Wigs For Kids Program. This program was new at the time and we have gone from very little marketing to an amazing array of strategies that have almost tripled our hair donations and online fundraising. This included an incredible events nights, updating our web site so it actually works for us instead of being just an online brochure, email marketing campaign to hairdressers - we are now set up to provide this service for years to come. Tara Beth Events continue to work with AAAF on new initiatives and assisting in increasing our membership.". ...
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ORCID: 0000-0001-8562-4944, Williams, J. A., Cole, Kathleen J., Muir, Gordon H., Grover, Philip L. and Phillips, David H. (2000) Susceptibility of primary cultures of human prostate epilthelial cells to chemical carcinogens as detected using the Comet assay. Mutagenesis, 15 (5). p. 447. ISSN 0267-8357 Full text not available from this repository.. Official URL: http://dx.doi.org/10.1093/mutage/15.5.431. ...
The idea that Im closer to 30 than my early 20s is both scary and exhilarating. I feel like this past year was a good one for so many reasons but also brought about a few struggles that I never pictured myself having to go through. Im confident that my time spent as a 28 year old will be a fabulous and come with many blessings and surprises! So in the spirit of that somewhat daunting number that now is associate with myself I thought I would share 28 things about me {wow, thats a lot of Kristin facts, sorry!} that you may not know or that I feel like define who I am really well. Let me know if any of them surprise you! ENJOY! xox. 1) Im the oldest of 4 girls…28, 25, 23 and 16.. 2) I have over 50 pairs of denim and they all fit.. 3) 80*+ is my ideal temperature.. 4) I graduated with my Bachelors degree from Iowa State in 3 years.. 5) I cannot keep plants or flowers alive no matter how hard I try.. 6) My dream vacation is Marrakech, Morocco.. 7) I could live with only 3 condiments: hot ...
The sensitivity of various methods suitable for biomonitoring the exposure to genotoxicants was compared in an animal model. The results were related to the presence of genotoxic effects in the target organ. Groups of male Wistar rats were given one oral dose of 0, 0.1, 1, 10 or 200 mg 2-acetylaminofluorene (2-AAF)/5 ml dimethyl sulphoxide/kg body weight. Peripheral blood cells, excreta, liver and spleen were collected at different time intervals after dosing. Mutagenicity in urine and extracts of faeces was determined using the Ames test with Salmonella typhimurium TA98 with and without S9 and with and without ??-glucuronidase. Genotoxic effects were studied by measuring DNA-adduct formation in lymphocytes, liver and spleen, and sister-chromatid exchanges (SCEs) in lymphocytes. DNA adducts were measured with immunochemical techniques and postlabelling methods. Mutagenecity in urine and faeces, collected during the first 24 h after treatment, was detected at 2-AAF doses of 1 mg/kg b.w. and ...
Carcinogen: Carcinogen, any of a number of agents that can cause cancer in humans. They can be divided into three major categories: chemical carcinogens (including those from biological sources), physical carcinogens, and oncogenic (cancer-causing) viruses. Most carcinogens, singly or in combination, produce
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Acetoxyacetylaminofluorene. ...
Acetoxyacetylaminofluorene Hydroxyacetylaminofluorene "NIOSH Pocket Guide to Chemical Hazards". Centers for Disease Control and ...
... acetoxyacetylaminofluorene MeSH D02.241.081.038.108.080.400 --- hydroxyacetylaminofluorene MeSH D02.241.081.038.108.189 --- ... acetoxyacetylaminofluorene MeSH D02.065.064.150.400 --- hydroxyacetylaminofluorene MeSH D02.065.064.189 --- ...
... acetoxyacetylaminofluorene MeSH D04.615.389.050.400 --- hydroxyacetylaminofluorene MeSH D04.615.389.850 --- tilorone MeSH ...
... is a derivative of 2-acetylaminofluorene used as a biochemical tool in the study of carcinogenesis. ...
Acetoxyacetylaminofluorene. *6-Acetoxydihydrotheaspirane. *Aceturic acid. *Acetyl bromide. *N-Acetylglutamic acid. *N- ...
Acetoxyacetylaminofluorene is a derivative of 2-acetylaminofluorene used as a biochemical tool in the study of carcinogenesis. ...
Acetoxyacetylaminofluorene Hydroxyacetylaminofluorene "NIOSH Pocket Guide to Chemical Hazards". Centers for Disease Control and ...
... acetoxy-acetylaminofluorene, even though the binding positions by these agents on guanines are different (25). The precise ...
Transformed cell foci were induced in hamster secondary cells after treatment for 6 days with acetoxyacetylaminofluorene, ...
... acetoxyacetylaminofluorene MeSH D02.241.081.038.108.080.400 --- hydroxyacetylaminofluorene MeSH D02.241.081.038.108.189 --- ... acetoxyacetylaminofluorene MeSH D02.065.064.150.400 --- hydroxyacetylaminofluorene MeSH D02.065.064.189 --- ...
... acetoxyacetylaminofluorene MeSH D04.615.389.050.400 --- hydroxyacetylaminofluorene MeSH D04.615.389.850 --- tilorone MeSH ...
... both at baseline and after a 2-acetoxyacetylaminofluorene (2-AAAF) challenge. In support of the in vivo data, As exposure ...
Marini, R. P., Anderson, J. L., Autio, W. R., Barritt, B. H., Cline, J. A., Cowgill, W. P., Crassweller, R. M., Domoto, P. A., Ferree, D. C., Garner, J., Gaus, A., Greene, G. M., Hampson, C., Hirst, P., Kushad, M. M., Mielke, E., Mullins, C. A., Parker, M., Perry, R. L., Privé, J. P. & 7 others, Reighard, G. L., Robinson, T., Rom, C. R., Roper, T. R., Schupp, J. R., Stover, E. & Unrath, R., Apr 1 2000, In : Journal of the American Pomological Society. 54, 2, p. 92-107 16 p.. Research output: Contribution to journal › Article ...
Acetoxyacetylaminofluorene. *6-Acetoxydihydrotheaspirane. *Aceturic acid. *Acetyl bromide. *N-Acetylglutamic acid. *N- ...
Acetoxyacetylaminofluorene *Hydroxyacetylaminofluorene *Allylisopropylacetamide *Iodoacetamide *Linezolid *Piracetam * ...
2-acetoxyacetylaminofluorene; 2-AAF, 2-acetyl aminofluorene; 2-AN, 2-aminoanthracene; 4-NQO, 4-nitroquinoline-N-oxide; 6TG, 6- ...
A specific 36-bp DNA sequence was either UV-irradiated or damaged by benzo(a)pyrene diol epoxide and N- acetoxy-acetylaminofluorene ...
Acetoxyacetylaminofluorene/pharmacology , Chromatography, Thin Layer , Codon , DNA Damage , Electrophoresis, Agar Gel , Genes, ... A molecularly cloned human cellular H-ras (c-H-ras) oncogene(pbc N1 plasmid) was treated with N-acetoxyacetylaminofluorene ( ... Identification of mutagenic site of c-H-ras oncogene damaged by N-acetoxyacetylaminofluorene(AAAF) ...
... pyrene diol epoxide and N-acetoxy-acetylaminofluorene. Cancer Lett. 2000, 158 (1): 17-25. 10.1016/S0304-3835(00)00517-6View ...
... both at baseline and after a 2-acetoxyacetylaminofluorene (2-AAAF) challenge. In support of the in vivo data, As exposure ... both at baseline and after a 2-acetoxyacetylaminofluorene (2-AAAF) challenge. In support of the in vivo data, As exposure ...
D2.241.755.80 Acetoxyacetylaminofluorene D2.241.81.38.108.80.70 D2.241.81.18.110.80.70 Acetrizoic Acid D2.241.223.100.140.100. ...
acetoxyacetylaminofluorene. acetoxycrenulatin. acetylaminofluorene. acetylaminofluorenes. ...
... acetosity acetosulfone acetosyringone acetotartrate acetous acid acetowhitening acetoxolone acetoxy acetoxyacetylaminofluorene ...
Acetoxyacetylaminofluorene [Chemical/Ingredient]. acetoxyacrylic acid ethyl ester. acetoxybutynylbithiophene deacetylase ...
Acetoxyacetylaminofluorene - pharmacology , Phosphorylation - physiology , Protein Kinases - metabolism , Protein Kinases - ...
Show more information about ACETOXYACETYLAMINOFLUORENE. Search for acetoxyacetylaminofluorene in: Wikipedia Wiktionary Google ...
N Acetoxy 2 acetylaminofluorene use Acetoxyacetylaminofluorene N Acetoxy N acetyl 2 aminofluorene use ... N-Acetoxy-2-acetylaminofluorene use Acetoxyacetylaminofluorene N-Acetoxy-N-acetyl-2-aminofluorene use ...
N Acetoxy 2 acetylaminofluorene use Acetoxyacetylaminofluorene N Acetoxy N acetyl 2 aminofluorene use ... N-Acetoxy-2-acetylaminofluorene use Acetoxyacetylaminofluorene N-Acetoxy-N-acetyl-2-aminofluorene use ...
N Acetoxy 2 acetylaminofluorene use Acetoxyacetylaminofluorene N Acetoxy N acetyl 2 aminofluorene use ... N-Acetoxy-2-acetylaminofluorene use Acetoxyacetylaminofluorene N-Acetoxy-N-acetyl-2-aminofluorene use ...

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