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- W3162892258 abstract "Polycyclic aromatic hydrocarbons (PAH) are suspect human lung carcinogens that are metabolically activated. Five human aldo-keto reductases [AKR1A1 (aldehyde reductase) and AKR1C1-AKR1C4] are implicated in this process since they oxidize PAH-trans-dihydrodiol proximate carcinogens to yield reactive and redox-active PAH-ortho-quinones. These ortho-quinones enter into futile redox-cycles to amplify reactive oxygen species (ROS) and cause DNA-lesions. AKR1C1 is highly overexpressed in non-small cell lung carcinoma patients (1) and in the human lung adenocarcinoma cell line A-549. AKR1C activity in these cells is sufficient to convert dimethylbenz[a]anthracene (DMBA)-3,4-diol to DMBA-3,4-dione. We show that AKR derived PAH ortho-quinones produce sufficient ROS to mutate the major lung tumor suppressor gene (p53) in vitro. These mutations eliminate the transcriptional competency of p53 in a yeast-reporter system and this change-in-function results from G to T transversions (p<0.001). These results suggest that AKRs may be involved in the etiology of human lung cancer." @default.
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- W3162892258 date "2003-10-13" @default.
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- W3162892258 title "Aldo-Keto Reductases and the Metabolic Activation of Polycyclic Aromatic Hydrocarbons" @default.
- W3162892258 doi "https://doi.org/10.1021/bk-2003-0865.ch006" @default.
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