Detail of "17117-34-9"

Reference

Nucleophilic substitution reactions on 3-bromo- and 3-nitrobenzanthrones

Nucleophilic substitution reactions on 3-bromo- and 3-nitrobenzanthrones. Vaidyanathan, T.; Seshadri, S. (Dyes Res. Lab., Univ. Dep. Chem. Technol., Bombay 400019, India). Dyes Pigm., 5(6), 431-6 (English) 1984. CODEN: DYPIDX. ISSN: 0143-7208. DOCUMENT TYPE: Journal CA Section: 41 (Dyes, Organic Pigments, Fluorescent Brighteners, and Photographic Sensitizers) Section cross-reference(s): 25 Reaction of 3-bromobenzanthrone [81-96-9] with different arylamines gave rise to 6-(arylamino)-3-bromobenzanthrones. Anomalous behavior was obsd. with 2-aminobenzothiazole [136-95-8], when the Br atom underwent displacement, and with thiourea [62-56-6], when 3-mercaptobenzanthrone [6409-45-6] was obtained. Reactions of 3-nitrobenzanthrone [17117-34-9], on the other hand, gave rise to 4-substituted amino derivs.

DNA damage and acute toxicity caused by the urban air pollutant 3-nitrobenzanthrone in rats: characterization of DNA adducts in eight different tissues and organs with synthesized standards

All Rights Reserved. DNA damage and acute toxicity caused by the urban air pollutant 3-nitrobenzanthrone in rats: characterization of DNA adducts in eight different tissues and organs with synthesized standards. Nagy, Eszter; Adachi, Shuichi; Takamura-Enya, Takeji; Zeisig, Magnus; Moeller, Lennart (Department of Biosciences and Nutrition at Novum, Karolinska Institutet, Huddinge, Swed.). Environmental and Molecular Mutagenesis, 47(7), 541-552 (English) 2006 Wiley-Liss, Inc. CODEN: EMMUEG. ISSN: 0893-6692. DOCUMENT TYPE: Journal CA Section: 4 (Toxicology) Section cross-reference(s): 59 3-Nitrobenzanthrone (3-NBA) is an urban air pollutant and rat lung carcinogen that is among the most potent mutagens yet tested in the Salmonella reversion assay. In the present study, 1 mg 3-NBA was administered orally to female F344 rats and DNA adduct formation was examd. in liver, lung, kidney and five sections of the gastrointestinal (GI) tract at 6 h, and 1, 2, 3, 5, and 10 days after administration. The DNA adduct patterns, analyzed by 32P-postlabelling followed by HPLC sepn., were similar in all tissues and organs. Five of the adduct peaks cochromatographed with synthesized DNA adduct stds. Three of these unequivocally detd. stds., dGp-C8-N-ABA, dGp-N2-C2-ABA, and dAp-N6-C2-ABA, were of the nonacetylated type, suggesting that at least part of the pathway for activation of 3-NBA proceeds through O-acetylation of the hydroxylamine intermediate. The two other DNA adduct stds., dGp-C8-C2-N-Ac-ABA, and dGp-N2-C2-N-Ac-ABA, were of the acetylated type, but there was some ambiguity in the characterization of these DNA adducts, since they varied inconsistently between samples and they also aligned with peaks found in controls. At 6 h after treatment, the level of DNA adducts was highest in glandular stomach (relative adduct labeling (RAL), ~70 adducts/108 normal nucleotides (NN)); adduct levels in this organ decreased at 24 h, but increased afterwards. DNA adduct levels in the majority of organs were characterized by an early increase (from 6 h to 3 days), which was followed by a decrease at 5 days and a max.There are some commonly used reagents with their cas registry numbers 626203-60-9 and 17117-34-9 in this article. level 10 days after administration (RAL ~120 adducts/108 NN for the lung, kidney and glandular stomach, ~80 adducts/108 NN for the forestomach and cecum, and ~40 adducts/108 NN for the liver, small intestine, and colon). This pattern was consistent with pathol. observations during autopsy showing high levels of tissue damage in the GI tract; the tissue damage included hemorrhages, loss of villous surface structure in the small intestine, as well as intestine fragility and edema of the adipose tissue around the GI-tract. Tissue damage decreased and DNA adduct levels increased at 10 days after administration. These observations suggest that 3-NBA not only exerts acute toxic effects, but that the bioavailability is affected by storage in tissues and later becomes available, resulting in the increased DNA adduct levels at the later time points of collection. .