Acetoxy-2-acetylaminofluorene

Poirier, M.C., Williams, G.M. and Yuspa, S.H. (1980). Effect of culture conditions cell type and species of origin on the distribution of acetylated and deacetylated deoxyguanosine C-8 adducts of A-acetoxy-2-acetylaminofluorene. Mol. Pharmacol. 18 581-587. 

Poirier MC, DeCicco BT, Lieberman MW. 1975. Nonspecific inhibition of DNA repair synthesis by tumor promotors in human diploid fibroblasts damage with N-acetoxy-2-acetylaminofluorene. Cancer Res 35 1392-1397. 

Huang, S.L. and Lieberman, M.W. (1978). Induction of 6-thioguanine resistance in human cells treated with N-acetoxy-2-acetylaminofluorene, Mutat. Res. 57,349. 

Ball, S. S. Quaranta, V. Shadravan, F. Walford, R. L. An ELISA for Detection of DNA-bound carcinogen using a monoclonal antibody to N-acetoxy-2-acetylaminofluorene-modified DNA. J. Immunol. M., 98 195-200. 1987. 

We have examined the consequences of inhibition of chromatin-associated poly(ADP-ribosylation) on individual reaction steps of DNA repair elicited by a number of different carcinogens. In this analysis we could identify at least two ADP-ribose dependent reaction steps in the process of DNA repair, while others were found unresponsive to inhibition of nuclear ADP-ribosylation. Thus, for example, the rate of resynthesis of repair patches as well as the rate of ligation were increased in hepatocytes recovering from alkylation damage, pyrimidine dimers or bulky lesions caused by the ultimate carcinogen N-acetoxy-2-acetylaminofluorene (NAcAAF) ([9], F.R. Althaus, unpublished observations). Despite this apparent stimulation of intermediate steps of DNA repair, the removal of guanine adducts of NAcAAF (dG-8-AAF) was incomplete under conditions of inhibited ADP-ribosylation activity (F.R. Althaus and M.C. Poirier, unpublished observations). 

Primary cultures of rat hepatocytes were incubated for 20 min with the radioactively labeled ultimate carcinogen N-acetoxy-2-acetylaminofluorene (AAAF), the carcinogen was removed, and the cells were showed to repair DNA damage for up to 3 hr. Within this repair period, excision of the bulky... 

The BALB/c 3T3 cell line developed by Aaronson and Todaro has been extensively used for studies with oncogenic viruses. More recently, clones of this cell line have been used to establish quantitative focus assays in which transformation was demonstrated with several polycyclic aromatic hydrocarbons, A -acetoxy-2-acetylaminofluorene, 4-nitroquinoline-l-oxide, afla-toxin Bi, and A -methyl-A/ -nitro-A -nitrosoguanidine. Foci were not observed with diethylnitrosamine, dimethylnitrosamine, or a number of noncarcinogens. 

FIGURE 6. Comparison of the cytotoxicity (loss of cloning ability) produced in different strains of human fibroblasts by exposure to iV-acetoxy-2-acetylaminofluorene (V-AcO-AAF), benzo[a]pyrene 4,5-oxide (BP 4,5-oxide), or 7,12-dimethylbenz[a]anthracene 5,6-oxide (DMBA 5,6-oxide). The procedures used are described in Section 2.2. 

H. F. Stich, R. H. San, J. A. Miller, and E. C. Miller, Various levels of DNA repair synthesis in xeroderma pigmentosum cells exposed to the carcinogens, V-hydroxy and V-acetoxy-2-acetylaminofluorene, Nature London) New Biol. 238, 9-10 (1972). 

V. M. Maher and J. E. Wessel, Mutations to azaguanine resistance induced in cultured diploid human fibroblasts by the carcinogen, A -acetoxy-2-acetylaminofluorene, Mutat. Res. 

Aminofluorene V-Hydroxy-2-aminofluorene 2-Nitrosofluorene 2-Acetylaminofluorene A -Hydroxy-A-(2-fluorenyl)acetamide 2-Diacetylaminofluorene iV-Acetoxy-2-acetylaminofluorene... 

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