Disease relevance of Chrysenex

• Here we further examined the roles of human liver P450 enzymes and the mechanism of activation of 6-aminochrysene by rat and human P450 enzymes in the Salmonella tester strains [1].

High impact information on Chrysenex

• Fecal metabolites were identified, based on comparison of their chromatographic characteristics with those of standards, as trans-1,2-dihydro-1,2-dihydroxy-6-NC, chrysene-5,6-quinone, and 6-aminochrysene (6-AC); the structure of the latter was further confirmed by mass spectrometry and UV spectral analysis [2].
• The rank order of binding affinities of these chemicals to the cytosolic Ah receptor (2,3,7,8-tetrachlorodibenzo-p-dioxin much greater than benzo[a]pyrene greater than benzo[a]anthracene greater than 6-aminochrysene much greater than phenobarbital) is not correlated with their effects on EGF binding capacity [3].
• In contrast, induction of umuC gene expression by 1, 8-dinitropyrene, 6-aminochrysene and 2-amino-3,5-dimethylimidazo[4, 5-f]quinoline was weaker in the NM6001 strain than in the NM6002 strain [4].
• Roles of different forms of cytochrome P450 in the activation of the promutagen 6-aminochrysene to genotoxic metabolites in human liver microsomes [1].
• Pentachlorophenol, an inhibitor of acetyltransferase activity, suppressed the activation of 6-aminochrysene in liver microsomes from phenobarbital-treated rats and from human samples HL-4, HL-13 and HL-18 but not HL-16 [1].

Biological context of Chrysenex

• Since 6-nitrochrysene and 6-aminochrysene have shown activity in carcinogenicity bioassays, we have begun an investigation of their metabolic activation pathways and the nature of the carcinogen-DNA adducts that may be formed [5].
• 6-Aminochrysene kinetics in isolated perfused liver [6].
• It is concluded that even after short-term exposure, black tea enhances the metabolism of 6-aminochrysene and that this is probably related to the up-regulation of hepatic CYP1A2 by the caffeine present in black tea [7].
• 3. Pre-treatment of rats with 6-aminochrysene markedly decreased the N-demethylation in vitro but significantly increased the hydroxylation and the O-demethylation [8].

Anatomical context of Chrysenex

• Liver microsomes from 18 different human samples catalyzed activation of 6-aminochrysene more efficiently in S. typhimurium NM2009 than in the original strain of S. typhimurium TA1535/pSK1002 [1].
• The cytosolic activation of 6-aminochrysene decreased in the presence of increasing amounts of microsomes [9].
• Human hepatic cytosol could convert 6-aminochrysene and 2-aminoanthracene to mutagens in the Ames test [9].
• The amount of 6-aminochrysene excreted in the feces of germfree mice within 48 h after treatment with a single i.p. dose of [3H]6-nitrochrysene (0.03 mumol/5 microliters/g body wt) was approximately 25% of that excreted in identically treated conventional mice [10].
• By microspectrofluorimetry on single living cells (murine fibroblasts 3T3), we have obtained monoexponential decreases of fluorescence intensity for benzo[a]pyrene (B[a]P) and 6-aminochrysene (6a-chrysene) metabolism [11].

Associations of Chrysenex with other chemical compounds

• Although these pulmonary-derived tissue homogenates have significant AHH activity and can metabolize Aflatoxin B1, 2-aminofluorene and 7, 8-dihydro-7,8-dihydroxybenzo(a)pyrene to mutagenic forms, these homogenates fail to activate both cigarette smoke condensate and the pro-mutagen, 6-aminochrysene [12].
• Mutagen-DNA adduct analysis indicated that cells treated with 6-aminochrysene in the presence of S9 or 6-nitrosochrysene in the absence of S9 contained an adduct pattern identical to that derived from the in vitro reaction of N-hydroxy-6-aminochrysene with calf-thymus DNA [13].
• 6-Aminochrysene (6-AC) and trans-1,2-dihydro-1,2-dihydroxy-6-aminochrysene (1,2-DHD-6-AC) were the most active mutagens in TA100 upon metabolic activation [14].
• 3-Aminochrysene, a mutagenic geometric isomer of the mutagenic and carcinogenic aromatic amine 6-aminochrysene, has been synthesized and its metabolic activation studied by characterization of the products formed from the reaction of metabolites with calf thymus DNA [15].

Gene context of Chrysenex

• Inclusion of purified rat epoxide hydrolase to the reconstituted system containing rat and human P4501A enzymes caused a decrease in the rates of 6-aminochrysene activation.(ABSTRACT TRUNCATED AT 400 WORDS)[1]

Analytical, diagnostic and therapeutic context of Chrysenex

• 2. The decline in blood levels of the antitumoral agent 6-aminochrysene was due to its distribution rather than to metabolism to polar metabolites, during liver perfusion experiments [6].

References