期刊
JOURNAL OF NEUROCHEMISTRY
卷 102, 期 3, 页码 867-877出版社
WILEY
DOI: 10.1111/j.1471-4159.2007.04599.x
关键词
benzo(a)pyrene; carcinogenesis; target organ toxicity; xenobiotic metabolism
资金
- NHLBI NIH HHS [R01 HL070921] Funding Source: Medline
- NIEHS NIH HHS [R01 ES009132] Funding Source: Medline
- NIMH NIH HHS [MH 70054] Funding Source: Medline
CYP1A 1, a cytochrome P450 enzyme, metabolizes polycyclic aromatic hydrocarbons to genotoxic metabolite(s) that bind to DNA and initiate carcinogenesis. RT-PCR amplification of the complete open reading frame of CYP1A1 generated an amplicon of 1593 bp having deletion of 87 bp of exon-6 that translated into functional P450 enzyme. Unlike wild type CYP1A1, exon 6 del CYP1A1 did not metabolize polycyclic aromatic hydrocarbons such as, benzo(a)pyrene to genotoxic, ultimate carcinogens that form DNA adducts. Exon 6 del CYP1A1 metabolized ethoxyresorufin (the classical substrate for CYP1A1) less efficiently compared with wild type CYP1A1 while pentoxy and benzyloxyresorufin (classical substrates for CYP2B) were dealkylated more efficiently. In silico docking
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