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1 etabolism of inhaled drugs and tobacco smoke procarcinogens.
2 , is essential for the bioactivation of many procarcinogens.
3 ltered metabolic activation of tobacco smoke procarcinogens.
4 reserved tissues of rodents treated with the procarcinogens.
5 of androgenic steroids and certain aromatic procarcinogens.
6 A13 (CYP2A13) activates the nicotine-derived procarcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-buta
7 nt in tobacco, and activation of the tobacco procarcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-buta
8 0s participate in xenobiotic detoxification, procarcinogen activation, and steroid hormone synthesis.
12 tivation of hexamethylphosphoramide, a nasal procarcinogen, and 2,6-dichlorobenzonitrile (DCBN), a he
13 ign of chemopreventive strategies is whether procarcinogen bioactivation in an extrahepatic target ti
16 the enzyme in tumors, in that activation of procarcinogens could lead to the accumulation of mutatio
18 been shown to be formed in DNA from various procarcinogens (e.g., acrolein, malonaldehyde, vinyl chl
19 tivate nicotine and activate tobacco-derived procarcinogens [e.g., 4-[methylnitrosamino]-1-(3-pyridyl
20 none, is one of the most potent and abundant procarcinogens found in tobacco and tobacco smoke, and g
21 ic aromatic hydrocarbons (PAHs), is a potent procarcinogen generated during the combustion of fossil
22 the dispositions of reactive metabolites of procarcinogens in humans, provided that exposures are ad
24 A2 can catalyze the bioactivation of several procarcinogens, indicating a potential role in chemical
26 P450 2W1 catalyzed the activation of several procarcinogens, particularly polycyclic hydrocarbon diol
28 mportant enzymes in the detoxication of many procarcinogens, serve as a mechanism of bioactivation of
29 of benzo[a]pyrene (B[a]P), an environmental procarcinogen that activates Cyp1a1 transcriptional resp
30 yclic amines (HCAs) found in cooked meat are procarcinogens that are metabolically activated by N-hyd
31 els should be applicable to studies on other procarcinogens that require P450-mediated metabolic acti
32 ertain hepatotoxic chemicals, including some procarcinogens, their ability to monooxygenate, and ther
35 key to block the conversion of environmental procarcinogens to their carcinogenic metabolites in both