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Chemical Compound Review:

AC1O4QHJ (2R,3S)-butane-1,2,3-triol; (5E,6E)-5...

Synonyms:

Luch, A. et al., Scates, D.K. et al., Hu, X. et al., Ding, J. et al., Khan, Q.A. et al., et al.

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Disease relevance of BENZO[G]CHRYSENE

Metabolic activation of benzo[g]chrysene in the human mammary carcinoma cell line MCF-7 [1].

High impact information on BENZO[G]CHRYSENE

In this communication, we report that the I104,A113 allele of hGSTP1-1, which is most frequent in human populations, is also most efficient in the GSH conjugation of carcinogenic anti-diol epoxides of benzo[g]chrysene and benzo[c]phenanthrene (anti-BGCDE and anti-BCPDE, respectively) [2].
The results established that the covalently attached benzo[g]chrysene ring intercalates into the DNA helix directed towards the 5'-side of the modified strand and stacks predominantly with dT17 when intercalated between dC5.dG18 and (B[g]C)dA6.dT17 base-pairs [3].
Synthesis of fjord region tetraols and their use in hepatic biotransformation studies of dihydrodiols of benzo[c]chrysene, benzo[g]chrysene and dibenzo[a,l]pyrene [4].
Under standardized conditions the acidic hydrolysis of syn-dihydrodiol epoxides of benzo[c]chrysene, benzo[g]chrysene and dibenzo[a,l]pyrene resulted in the formation of two tetraols with cis/trans ratios of 81:19, 77:23 and 80:20, respectively, whereas the anti-dihydrodiol epoxides underwent almost exclusively trans hydrolysis [4].
The effect of a potent mammary carcinogen, anti benzo[g]chrysene 11,12-dihydrodiol 13,14-epoxide, on the progress of human mammary carcinoma MCF-7 cells through the cell cycle was investigated [5].

Anatomical context of BENZO[G]CHRYSENE

Capillary electrochromatography (CEC) was used for the analysis of mixtures of neutral isomeric compounds derived from the reaction of carcinogenic hydrocarbon (benzo[g]chrysene and 5,6-dimethylchrysene) dihydrodiol epoxides with calf thymus deoxyribonucleic acid (DNA) [6].

Associations of BENZO[G]CHRYSENE with other chemical compounds

32P-Postlabeling assays showed that MCL-5 cells (genetically engineered to express five human cytochromes P450 and microsomal epoxide hydrolase) formed characteristic adduct spots with benz[a]pyrene, benzo[g]chrysene, 7,12-dimethylbenz[a]anthracene, benzidine, sterigmatocystin and 3-methylcholanthrene, whereas CCRF cells did not [7].

Gene context of BENZO[G]CHRYSENE

DNA adduct levels associated with p53 induction and delay of MCF-7 cells in S phase after exposure to benzo[g]chrysene dihydrodiol epoxide enantiomers [8].
Similarly, induction of p53 also required a higher dose of benzo[g]chrysene 11S, 12R-dihydrodiol 13R, 14S-epoxide [8].

References

Metabolic activation of benzo[g]chrysene in the human mammary carcinoma cell line MCF-7. Agarwal, R., Coffing, S.L., Baird, W.M., Kiselyov, A.S., Harvey, R.G., Dipple, A. Cancer Res. (1997) [Pubmed]
Catalytic efficiencies of allelic variants of human glutathione S-transferase P1-1 toward carcinogenic anti-diol epoxides of benzo[c]phenanthrene and benzo[g]chrysene. Hu, X., Xia, H., Srivastava, S.K., Pal, A., Awasthi, Y.C., Zimniak, P., Singh, S.V. Cancer Res. (1998) [Pubmed]
Solution conformation of the (+)-trans-anti-benzo[g]chrysene-dA adduct opposite dT in a DNA duplex. Suri, A.K., Mao, B., Amin, S., Geacintov, N.E., Patel, D.J. J. Mol. Biol. (1999) [Pubmed]
Synthesis of fjord region tetraols and their use in hepatic biotransformation studies of dihydrodiols of benzo[c]chrysene, benzo[g]chrysene and dibenzo[a,l]pyrene. Luch, A., Platt, K.L., Seidel, A. Carcinogenesis (1998) [Pubmed]
Cellular response to DNA damage from a potent carcinogen involves stabilization of p53 without induction of p21(waf1/cip1). Khan, Q.A., Vousden, K.H., Dipple, A. Carcinogenesis (1997) [Pubmed]
Application of mixed mobile phases and a step gradient method in capillary electrochromatography for the separation of isomeric polycyclic aromatic hydrocarbon-deoxyribonucleoside adduct mixtures prepared in vitro. Ding, J., Szeliga, J., Dipple, A., Vouros, P. Journal of chromatography. A. (1997) [Pubmed]
Differences in the levels and pattern of DNA-adduct labelling in human cell lines MCL-5 and CCRF, proficient or deficient in carcinogen-metabolism, treated in vitro with bile from familial adenomatous polyposis patients and from unaffected controls. Scates, D.K., Spigelman, A.D., Phillips, R.K., Venitt, S. Carcinogenesis (1996) [Pubmed]
DNA adduct levels associated with p53 induction and delay of MCF-7 cells in S phase after exposure to benzo[g]chrysene dihydrodiol epoxide enantiomers. Khan, Q.A., Agarwal, R., Seidel, A., Frank, H., Vousden, K.H., Dipple, A. Mol. Carcinog. (1998) [Pubmed]

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