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• W1455139017 abstract "Proc Amer Assoc Cancer Res, Volume 45, 2004762 Tobacco smoke contains an abundance of oxidants and free radicals, which, in addition to carcinogens such as polycyclic aromatic hydrocarbons and tobacco specific nitrosamines (TSNAs), are thought to play a role in lung carcinogenesis and be responsible for the observed depletion of blood antioxidants in smokers. Results from epidemiological, clinical intervention and laboratory studies indicate a protective role for selenium against several cancers including lung cancer. In one trial, Se-enriched yeast (Se-yeast) protected against lung cancer in individuals with low baseline levels of plasma Se. We hypothesize that one mechanism for Se chemoprevention is inhibition of oxidative damage to critical macromolecules by inducing antioxidant enzymes and/or levels of antioxidants especially in target organs. To test this, we determined (1) if antioxidants in the lung are depleted in NNK treated mice in relation to tumor formation and (2) whether Se (p-XSC or Se-yeast) is effective at preventing these changes. A/J mice (5 wk old) were fed either control or experimental (containing 10 ppm p-XSC or Se-yeast) diets and, beginning at wk 7, received NNK (3 μmol in 0.1 ml cottonseed oil) by gavage once weekly for 8 wk. Mice were sacrificed 26 wk after NNK initiation and lungs were analyzed for tumor multiplicity and antioxidant content. p-XSC significantly reduced NNK-induced tumor burden by 74% (10.4 ± 6.0 vs 2.7 ± 1.5 tumors/mouse, P<0.001) and decreased tumor incidence from 96% to 68% (P<0.01), whereas Se- yeast had no effect. P-XSC was nearly 10-fold more effective at enhancing lung Se than was Se-yeast (P<0.01). Decreases in ascorbate levels ranging from 15% to 25% were observed in NNK-treated mice (P<0.05). In mice administered both NNK and p-XSC, ascorbate levels were increased 45% over NNK-treated alone (P<0.01), whereas p-XSC alone had no effect. Glutathione (GSH) levels in lung were unchanged in NNK-treated mice but were increased 72-75% in mice treated with a both NNK and p-XSC (P<0.01) and 42% in mice treated with p-XSC alone. Cyst(e)ine (Cys + cysteine) levels were decreased 18% in NNK-treated mice (P<0.02), but were increased about 2-fold in mice treated with either NNK and p-XSC in combination or with p-XSC alone (P<0.001). Se-yeast had no effect on antioxidant levels in either control or NNK-treated mice. These results demonstrate that NNK-induced tumorigenesis is associated with decreased ascorbate levels and indicate that inhibition of lung carcinogenesis by p-XSC is correlated with increased antioxidant levels. Altogether, these findings support the hypothesis that Se, in the form of p-XSC, inhibits tumor formation, in part, by protecting against oxidative damage, possibly through induction of lung GSH. Supported by NIH grants CA70972 and CA17613." @default.
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• W1455139017 date "2004-04-01" @default.
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• W1455139017 title "Effects of 4-(Methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) and selenium (1,4-Phenylenebis(methylene)selenocyanate, p-XSC, or selenium-enriched yeast) on tumorgenesis and antioxidant levels in A/J mouse lung" @default.
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