The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
MeSH Review

Bay Region (Chemistry)

Welcome! If you are familiar with the subject of this article, you can contribute to this open access knowledge base by deleting incorrect information, restructuring or completely rewriting any text. Read more.

Disease relevance of Bay Region (Chemistry)

  • The effects of bay-region methyl substitution on 6-nitrochrysene mutagenicity in Salmonella typhimurium and tumorigenicity in newborn mice [1].
  • This study was designed to evaluate the point mutations in the murine c-Ha-ras gene of skin papillomas induced by initiation with dibenz[a,j]anthracene (DB[a,j]A), its bay-region anti-diol epoxide ((+/-)anti-DB[a,j]A-DE), and a 7,14-dimethyl analogue (7,14-diMeDB[a,j]A) [2].
  • The molecular distortion in the Pbca polymorph is also larger than that in the Pnaa polymorph; this distortion is evidenced by torsion angles (13-20 degrees) in the bay region and by an out-of-plane displacement (0.8 A) of the C atom of the methylene portion of the ethyl group [the C atom attached to C(11)] [3].

High impact information on Bay Region (Chemistry)

  • We report here that DNA adducts formed from benzo[a]pyrene bay-region diol epoxides can markedly affect top1 activity [4].
  • The tumorigenicity results reported here are the first direct demonstration that conformation of the hydroxyl groups in a bay-region diol epoxide, in addition to the documented effect of absolute configuration, is an important determinant in the tumorigenic activity of these ultimate carcinogens [5].
  • Collectively, these results indicate that the adenine adducts induced by both bay-region diol epoxides of DMBA lead to the mutation at codon 61 of H-ras and, consequently, initiate tumorigenesis in mouse skin [6].
  • Major metabolites of 6-MeC were 6-MeC-1,2-diol, bay region dihydrodiols, phenols, and 6-(hydroxymethyl)chrysene [7].
  • Tannic acid inhibits the mutagenicity of several polycyclic aromatic hydrocarbons (PAHs) and their bay-region diol-epoxides [8].

Chemical compound and disease context of Bay Region (Chemistry)


Biological context of Bay Region (Chemistry)

  • These results suggest that methylation of BA at C-7 greatly enhances the oxidation of the 3S,4S-dihydrodiol, while the presence of a bay-region methyl group at C-12 completely blocks the oxidation of the 3R,4R-stereoisomer [11].
  • The results show that both major adducts have chromatographic properties identical to those of adducts formed when r-1,t-2-dihydroxy-t-3,4-oxy-1,2,3,4-tetrahydrochrysene reacts with DNA and provide evidence that metabolic activation of chrysene occurs via the formation of this 'bay-region' diol-epoxide [12].
  • Several groups used the UvrABC endonuclease incision assay to demonstrate that methylated CG dinucleotides of the p53 gene are the preferred binding sites for the diol epoxides of bay region polycyclic aromatic hydrocarbons (PAH) [13].
  • The 3'-monophosphates of the major deoxyribonucleoside adducts of five representative polynuclear aromatic hydrocarbons (PAH)-benzo[a]pyrene, benz[a]anthracene, chrysene, 5-methylchrysene and 6-methylchrysene--were prepared by reaction with DNA of the appropriate bay-region diol epoxides followed by enzymatic hydrolysis and HPLC purification [14].
  • Three different modes of cytotoxicity were observed: (1) NPQ (no bay region) and DMBAQ (methylated bay region) were as cytotoxic as menadione in reducing cell survival but had less effect on cell viability [15].

Anatomical context of Bay Region (Chemistry)

  • Substitution with fluorine at C-6 caused an almost 2.5-fold increase in the percentages of the putative proximate carcinogens, i.e. benzo-ring dihydrodiols with bay-region double bonds, when liver microsomes from 3-methylcholanthrene-treated rats were used [16].
  • Aroclor 1254-induced microsomes were the most effective metabolisers of this compound, the major metabolites being oxidation products of the bay region A ring [17].

Associations of Bay Region (Chemistry) with chemical compounds

  • The results of this study show that the high tumorigenicity of 5-MeC compared to 6-MeC is due to the remarkable tumorigenic activity of 5-MeC-1R,2S-diol-3S,4R-epoxide which, in contrast to 6-MeC-1R,2S-diol-3S,4R-epoxide, has a methyl group in the same bay region as the epoxide ring [18].
  • Evidence for bay region activation of chrysene 1,2-dihydrodiol to an ultimate carcinogen [19].
  • For identification of these products, markers were prepared from 5-methylchrysene bay-region dihydrodiol epoxides [20].
  • Tumorigenicity of bay-region epoxides and other derivatives of chrysene and phenanthrene in newborn mice [21].
  • Among the R,S,S,R enantiomers, 5-MeC-1,2-diol-3,4-epoxide, which has a methyl group in the same bay region as the epoxide ring, was most reactive toward DNA, and in particular toward dGuo [22].

Gene context of Bay Region (Chemistry)

  • With GSTM1-1, the bay-region diol epoxides, in particular the syn-diastereomers were in most cases more efficiently conjugated with GSH than the fjord-region analogues [23].
  • We have determined the tumor-initiating activity of (+/-)syn- and (+/-)anti-7,12-dimethylbenz[a]anthracene-3,4-diol-1,2-epoxide (syn- and anti-DMBADE), the two metabolically formed bay-region diol epoxides of DMBA, and we have also analyzed mutations in the H-ras gene from tumors induced by these compounds [6].
  • Consistent with earlier studies of other PAH, calculations by the INDO method of the ease of carbon cation formation from a bay region diol epoxide yielded a set of values which gave a good correlation with carcinogenicity [24].
  • These studies indicate that tumorigenic activity of methylated phenanthrenes requires inhibition of dihydrodiol formation at the K-region (9,10-positions) in addition to a bay-region methyl group and a free peri position, both adjacent to an unsubstituted angular ring [25].
  • On the basis of this structural information, new catalysts were prepared in which the "bay region" tert-butyl groups were replaced by trimethylsilyl groups [26].

Analytical, diagnostic and therapeutic context of Bay Region (Chemistry)

  • However, analysis of DMBA--DNA adducts by Servacel DHB chromatography and high-pressure liquid chromatography showed that treatment of cells with BHA, but not with BHT, resulted in a decreased contribution from the syn bay region dihydrodiol epoxide to overall binding [27].


  1. The effects of bay-region methyl substitution on 6-nitrochrysene mutagenicity in Salmonella typhimurium and tumorigenicity in newborn mice. el-Bayoumy, K., Shiue, G.H., Amin, S., Hecht, S.S. Carcinogenesis (1989) [Pubmed]
  2. Analysis of point mutations in murine c-Ha-ras of skin tumors initiated with dibenz[a,j]anthracene and derivatives. Gill, R.D., Beltrán, L., Nettikumara, A.N., Harvey, R.G., Kootstra, A., DiGiovanni, J. Mol. Carcinog. (1992) [Pubmed]
  3. C-H...O packing motifs in some cyclopenta[a]phenanthrenes. Desiraju, G.R., Kashino, S., Coombs, M.M., Glusker, J.P. Acta Crystallogr., B (1993) [Pubmed]
  4. Benzo[a]pyrene diol epoxide adducts in DNA are potent suppressors of a normal topoisomerase I cleavage site and powerful inducers of other topoisomerase I cleavages. Pommier, Y., Kohlhagen, G., Pourquier, P., Sayer, J.M., Kroth, H., Jerina, D.M. Proc. Natl. Acad. Sci. U.S.A. (2000) [Pubmed]
  5. Role of diaxial versus diequatorial hydroxyl groups in the tumorigenic activity of a benzo[a]pyrene bay-region diol epoxide. Chang, R.L., Wood, A.W., Conney, A.H., Yagi, H., Sayer, J.M., Thakker, D.R., Jerina, D.M., Levin, W. Proc. Natl. Acad. Sci. U.S.A. (1987) [Pubmed]
  6. Both (+/-)syn- and (+/-)anti-7,12-dimethylbenz[a]anthracene-3,4-diol-1,2-epoxides initiate tumors in mouse skin that possess -CAA- to -CTA- mutations at Codon 61 of c-H-ras. Tang, M.S., Vulimiri, S.V., Viaje, A., Chen, J.X., Bilolikar, D.S., Morris, R.J., Harvey, R.G., Slaga, T.J., DiGiovanni, J. Cancer Res. (2000) [Pubmed]
  7. Metabolism of 5-methylchrysene and 6-methylchrysene by human hepatic and pulmonary cytochrome P450 enzymes. Koehl, W., Amin, S., Staretz, M.E., Ueng, Y.F., Yamazaki, H., Tateishi, T., Guengerich, F.P., Hecht, S.S. Cancer Res. (1996) [Pubmed]
  8. Effect of dietary tannic acid on epidermal, lung, and forestomach polycyclic aromatic hydrocarbon metabolism and tumorigenicity in Sencar mice. Athar, M., Khan, W.A., Mukhtar, H. Cancer Res. (1989) [Pubmed]
  9. Mutagenicity in Salmonella and sister chromatid exchange in mice for the bay-region syn- and anti-diol epoxides of 1,4-dimethylphenanthrene. Sinsheimer, J.E., Giri, A.K., Messerly, E.A., Jung, K.Y., Koreeda, M. Carcinogenesis (1989) [Pubmed]
  10. Methylene-bridged bay region chrysene and phenanthrene derivatives and their keto-analogs: mutagenicity in Salmonella typhimurium and tumor-initiating activity on mouse skin. Rice, J.E., Makowski, G.S., Hosted, T.J., Lavoie, E.J. Cancer Lett. (1985) [Pubmed]
  11. Oxidation of the trans-3,4-dihydrodiol metabolites of the potent carcinogen 7,12-dimethylbenz(a)anthracene and other benz(a)anthracene derivatives by 3 alpha-hydroxysteroid-dihydrodiol dehydrogenase: effects of methyl substitution on velocity and stereochemical course of trans-dihydrodiol oxidation. Smithgall, T.E., Harvey, R.G., Penning, T.M. Cancer Res. (1988) [Pubmed]
  12. The metabolic activation of chrysene by hamster embryo cells. Hodgson, R.M., Pal, K., Grover, P.L., Sims, P. Carcinogenesis (1982) [Pubmed]
  13. Endogenous 5-methylcytosine protects neighboring guanines from N7 and O6-methylation and O6-pyridyloxobutylation by the tobacco carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone. Ziegel, R., Shallop, A., Upadhyaya, P., Jones, R., Tretyakova, N. Biochemistry (2004) [Pubmed]
  14. Chromatographic conditions for separation of 32P-labeled phosphates of major polynuclear aromatic hydrocarbon--deoxyribonucleoside adducts. Amin, S., Misra, B., Desai, D., Huie, K., Hecht, S.S. Carcinogenesis (1989) [Pubmed]
  15. Cytotoxicity of polycyclic aromatic hydrocarbon o-quinones in rat and human hepatoma cells. Flowers-Geary, L., Harvey, R.G., Penning, T.M. Chem. Res. Toxicol. (1993) [Pubmed]
  16. Oxidative metabolism of the carcinogen 6-fluorobenzo[c]phenanthrene. Effect of a K-region fluoro substituent on the regioselectivity of cytochromes P-450 in liver microsomes from control and induced rats. Prasad, G.K., Mirsadeghi, S., Boehlert, C., Byrd, R.A., Thakker, D.R. J. Biol. Chem. (1988) [Pubmed]
  17. The metabolism and activation of 15,16-dihydrocyclopenta[a]phenanthren-17-one by cytochrome P-450 proteins. Boyd, G.W., Young, R.J., Harvey, R.G., Coombs, M.M., Ioannides, C. Eur. J. Pharmacol. (1993) [Pubmed]
  18. Enhancing effect of a bay region methyl group on tumorigenicity in newborn mice and mouse skin of enantiomeric bay region diol epoxides formed stereoselectively from methylchrysenes in mouse epidermis. Hecht, S.S., Amin, S., Huie, K., Melikian, A.A., Harvey, R.G. Cancer Res. (1987) [Pubmed]
  19. Evidence for bay region activation of chrysene 1,2-dihydrodiol to an ultimate carcinogen. Levin, W., Wood, A.W., Chang, R.L., Yagi, H., Mah, H.D., Jerina, D.M., Conney, A.H. Cancer Res. (1978) [Pubmed]
  20. Influence of bay-region methyl group on formation of 5-methylchrysene dihydrodiol epoxide:DNA adducts in mouse skin. Melikian, A.A., LaVoie, E.J., Hecht, S.S., Hoffmann, D. Cancer Res. (1982) [Pubmed]
  21. Tumorigenicity of bay-region epoxides and other derivatives of chrysene and phenanthrene in newborn mice. Buening, M.K., Levin, W., Karle, J.M., Yagi, H., Jerina, D.M., Conney, A.H. Cancer Res. (1979) [Pubmed]
  22. Reactivity with DNA bases and mutagenicity toward Salmonella typhimurium of methylchrysene diol epoxide enantiomers. Melikian, A.A., Amin, S., Huie, K., Hecht, S.S., Harvey, R.G. Cancer Res. (1988) [Pubmed]
  23. Glutathione conjugation of bay- and fjord-region diol epoxides of polycyclic aromatic hydrocarbons by glutathione transferases M1-1 and P1-1. Sundberg, K., Widersten, M., Seidel, A., Mannervik, B., Jernström, B. Chem. Res. Toxicol. (1997) [Pubmed]
  24. Quantum chemical studies of methyl and fluoro analogs of chrysene: metabolic activation and correlation with carcinogenic activity. Poulsen, M.T., Loew, G.H. Cancer Biochem. Biophys. (1981) [Pubmed]
  25. Tumor-initiating activity and metabolism of polymethylated phenanthrenes. LaVoie, E.J., Bedenko, V., Tulley-Freiler, L., Hoffmann, D. Cancer Res. (1982) [Pubmed]
  26. Design and development of highly effective Lewis acid catalysts for enantioselective Diels-Alder reactions. Huang, Y., Iwama, T., Rawal, V.H. J. Am. Chem. Soc. (2002) [Pubmed]
  27. Effects of butylated hydroxyanisole and butylated hydroxytoluene on 7,12-dimethylbenz[a]anthracene-DNA adduct formation in mouse embryo cell cultures. Sawicki, J.T., Dipple, A. Cancer Lett. (1983) [Pubmed]
WikiGenes - Universities