| 标题 |
[高分]
 Formation of Benzo[a]pyrene Diol Epoxide−DNA Adducts at Specific Guanines within K-ras and p53 Gene Sequences: Stable Isotope-Labeling Mass Spectrometry Approach† |
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| 其它 | he mutagenicity of a prominent tobacco carcinogen, benzo[a]pyrene (B[a]P), is believed to result from chemical reactions between its diol epoxide metabolite, (+)-anti-7r,8t-dihydroxy-c9,10-epoxy-7,8,9,10-tetrahydrobenzo[a]pyrene (BPDE), and DNA, producing promutagenic lesions, e.g., (+)-trans-anti-7R,8S,9S-trihydroxy-10S-(N2-deoxyguanosyl)-7,8,9,10-tetrahydrobenzo[a]pyrene (N2-BPDE-dG). Previous studies used the DNA repair enzyme UvrABC endonuclease in combination with ligation-mediated PCR (LMPCR) to demonstrate an increased reactivity of BPDE toward guanine nucleobases within codons 157, 248, and 273 of the p53 tumor suppressor gene (Denissenko, M. F., Pao, A., Tang, M., and Pfeifer, G. P. Science274, 430−432). These sites are also “hot spots” for mutations observed in lung tumors of smokers, suggesting an involvement of B[a]P in the initiation of lung cancer. |
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