Disease relevance of chrysene

• The ability of prostaglandin synthetase (PGS) to cooxidize benzo(a)pyrene, benzo(a)anthracene, chrysene, and several of their dihydrodiol derivatives to mutagenic products was tested with Salmonella typhimurium strains TA98 and TA100 [1].
• In this study, the enzymes involved in polycyclic aromatic hydrocarbon (PAH) degradation in the chrysene-degrading organism Sphingomonas sp. strain CHY-1 were investigated [2].
• As part of a systematic analysis of mechanisms of PAH developmental toxicity in zebrafish, we show here that three tetracyclic PAHs (pyrene, chrysene, and benz[a]anthracene) activate the AHR pathway tissue-specifically to induce distinct patterns of CYP1A expression [3].
• Singlet oxygen was generated at room temperature in the solutions via photosensitization of sodium chrysene sulfonate; this sulfonated polycyclic hydrocarbon was synthesized to provide a water soluble chromophore inert to usual dye-ascorbate photobleaching [4].
• At a concentration of 6.8 microM, F23Q also substantially inhibited the mineralization of benz[a]anthracene, benzo[a]pyrene (BaP), and chrysene by strain R1 as well as BaP mineralization by Pseudomonas saccharophila P15 [5].

High impact information on chrysene

• Comparison of the uptake rate of chrysene from the unperturbed crystal state, sonicated crystals, and the silica-adsorbed state demonstrated that the last condition results in the most rapid transport of chrysene into model membranes [6].
• METHODS: Here we have mapped the distribution of adducts induced by diol epoxides of additional PAHs: chrysene (CDE), 5-methylchrysene (5-MCDE), 6-methylchrysene (6-MCDE), benzo[c]phenanthrene (B[c]PDE), and benzo[g]chrysene (B[g]CDE) within exons 5, 7, and 8 of the p53 gene in human bronchial epithelial cells [7].
• Specificity analysis of the antibodies demonstrated that serological cross-reactions between the benzo[a]pyrene and the chrysene diol-epoxide adducts were present [8].
• Hydrolysis with trypsin and pronase gave products with the characteristic UV spectrum of substituted chrysene [9].
• All autoradiograms of DNA from fish from the contaminated sites exhibited a diagonal radioactive zone where DNA adducts of chrysene, benzo(a)pyrene, and dibenz(a,h)anthracene, formed in vitro using English sole hepatic microsomes, were shown to chromatograph [10].

Chemical compound and disease context of chrysene

• The K-region oxides and imines of chrysene, benzo[c]phenanthrene and benzo[g]chrysene were investigated for mutagenicity in Salmonella typhimurium TA98 and TA100, using two different exposure media [11].
• Methylene-bridged bay region chrysene and phenanthrene derivatives and their keto-analogs: mutagenicity in Salmonella typhimurium and tumor-initiating activity on mouse skin [12].
• Metabolic responses to short-term acute toxicities of naphthalene, anthracene, and chrysene were investigated in the freshwater bivalve mollusk Elliptio complanata using differential scanning calorespirometry coupled with uptake and scanning electron microscopy [13].
• The toxicity of benzo[a]pyrene, chrysene, and fluorene and their decomposition products formed by advanced oxidation processes (AOPs) was investigated using biotests with Escherichia coli and Vibrio fischeri [14].
• The mutagenic activity of four 4,5-bridged chrysene derivatives, benz(a)aceanthrylene, and 5-methylchrysene was examined using histidine auxotrophic strains TA98 and TA100 of Salmonella typhimurium [15].

Biological context of chrysene

• Evidence for bay region activation of chrysene 1,2-dihydrodiol to an ultimate carcinogen [16].
• Metabolic activation of chrysene in mouse skin appears to involve r-1,t-2-dihydroxy-t-3,4-oxy-1,2,3,4-tetrahydrochrysene (anti-chrysene-1,2-diol 3,4-oxide) and 9-hydroxy-r-1,t-2-dihydroxy-t-3,4-oxy-1,2,3,4-tetrahydrochrysene (anti-9-OH-chrysene-1,2-diol 3,4-oxide) [17].
• Adducts derived from the covalent binding of two positional monomethyl-substituted isomers of a bay region chrysene diol epoxide to supercoiled pIBI30 DNA (2926 base pairs/genome) were prepared, and their characteristics were investigated by a combination of gel electrophoresis and flow linear dichroism techniques [18].
• The kinetics of chrysene loss are first order in chrysene [19].
• The early ozonation mixture, 1.75 mol O3/mol Chr, exhibited greater inhibition to GJIC than chrysene and irreversible damage to cells leading to cell death [20].

Anatomical context of chrysene

• Stereoselective metabolism of chrysene by rat liver microsomes. Direct separation of diol enantiomers by chiral stationary phase h.p.l.c [21].
• Two nitroaromatics, 6-nitrobenzo[a]pyrene (6-N-BaP) and 6-nitrochrysene (6-N-CRY), and the corresponding parent hydrocarbons, benzo[a]pyrene (BaP) and chrysene (CRY), were studied in in vitro transformation assays with Syrian hamster embryo (SHE) cells, BALB/3T3 and C3H10T1/2 mouse cell lines [22].
• DACs- and chrysene-induced mutation in all of the six organs examined (liver, spleen, lung, kidney, bone marrow and colon) [23].
• Mutagenicity tests were performed with chrysene in the Salmonella/microsome test, NMRI-mice oocytes, bone-marrow cells and spermatogonia of Chinese hamsters [24].
• Lethality and EROD-inducing potency of chlorinated chrysene in chick embryos [25].

Associations of chrysene with other chemical compounds

• Tumorigenicity of bay-region epoxides and other derivatives of chrysene and phenanthrene in newborn mice [26].
• The rates of hydrolysis in the absence and presence of native and denatured DNA, and the extents of DNA binding of five dihydrodiol epoxides derived from 5-methylchrysene (5-MeC) and chrysene have been determined [27].
• These studies indicate that the presence and orientation of the hydroxyl groups play an important role in modulating the mutagenic activity of bay-region epoxides of chrysene in both bacterial and mammalian cells [28].
• Mono- and diphenols of chrysene and benzo(a)pyrene are suspected substrates of a 3-methylcholanthrene (MC)-inducible phenol UDP-glucuronosyltransferase (UGT1A1) [29].
• Five nitrated polycyclic aromatic hydrocarbons, synthesized from benzo[a]pyrene, fluoranthene, pyrene, and chrysene induced dose-dependent transformation of Syrian hamster embryo cells [30].

Gene context of chrysene

• None of the 14 PAHs bound the hrER, but five of the PAHs (anthracene, B[a]A, chrysene, B[b]F, and B[a]P) induced ER-reporter activity [31].
• 6-Nitrochrysene induced CYP1 mRNAs to the same extent or more potently than chrysene [32].
• Treatment of the Caco-2 cells with B[a]P, chrysene, B[k]F, or DB[a,l]P induced mRNA expression of CYP1A1 and CYP1B1 specifically as measured by RT-PCR [33].
• Mono- and Diglucuronide formation from benzo[a]pyrene and chrysene diphenols by AHH-1 cell-expressed UDP-glucuronosyltransferase UGT1A7 [34].
• V79 cell-expressed rat UGT1A6 also catalyzed these reactions, except for chrysene diphenol diglucronide formation (Bock et al., Mol Pharmacol 42: 613-618, 1992) [34].

Analytical, diagnostic and therapeutic context of chrysene

• The presence of serum antibodies to the diol-epoxide DNA adducts of representative polycyclic aromatic hydrocarbons (PAH), chrysene, benz[a]anthracene and benzo[a]pyrene, was determined by ELISA using serum samples obtained from normal healthy individuals [8].
• The enantiomers of chrysene 1,2-epoxide and 3,4-epoxide were also resolved by chiral stationary phase HPLC [35].
• Results from these bioassays indicate that methylene-bridged bay-region derivatives of chrysene and benz[a]anthracene contribute to the overall genotoxicity of environmentally occurring PAHs [36].
• The separation of monohydroxylated derivatives (phenols) of benzo[a]pyrene, benz[a]anthracene, and chrysene was studied by reversed-phase high-performance liquid chromatography using a monomeric Zorbax ODS column and a polymeric Vydac C18 column [37].
• Induction of TG resistance was also observed in P3 cells cocultivated in a cell-mediated assay with human breast carcinoma cells, which are capable of polycyclic aromatic hydrocarbon (PAH) metabolism, after treatment with the carcinogenic PAHs: B[a]P, chrysene, 7,12-dimethylbenz[a]anthracene (DMBA), and 3-methylcholanthrene (MCA) [38].

References