Synergistic induction of DNA strand breakage by cigarette tar and nitric oxide

Yoshie, Yumiko; Ohshima, Hiroshi

doi:10.1093/carcin/18.7.1359

Cited by 77 publications

(41 citation statements)

References 4 publications

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“…A determinação do EOT fornece um indício preciso de peroxidação lipídica e de estresse oxidativo 17,19 . Tem-se afirmado que o aumento na produção de espécies reativas de oxigênio associado ao fumo pode exceder a capacidade do sistema de defesa oxidante, resultando em dano oxidativo a certas proteínas, lipídios e ao DNA 23,28 . Em lactentes expostos ao tabagismo passivo, vários componentes do sistema de defesa antioxidante foram apontados como deficientes, se comparados aos dos lactentes não expostos ao tabagismo passivo 2,9,19,29 .…”

Section: Resultsunclassified

Increased oxidative stress in preschool children exposed to passive smoking

et al. 2011

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Objectives: To study the effect of passive cigarette smoking on plasma oxidative and antioxidative status in passive smoking preschool children and to compare them with controls.Methods: Thirty-four passive smoking (five to 50 cigarettes per day) preschool children (study group) and 32 controls who had never been exposed to cigarette smoke were randomly chosen from children aged from 4 to 6 years. Urinary cotinine and plasma indicators of oxidative and antioxidative status, i.e., total oxidant status (TOS), total antioxidant capacity (TAC), and oxidative stress index (OSI), were determined.Results: Mean environmental cigarette consumption was 22±13 cigarettes per day in passive smoking children. Mean urinary cotinine levels were 77.6±41.4 ng/mL and 11.9±2.3 ng/mL in the study and control groups, respectively (p < 0.001). Mean plasma TAC levels were 0.95±0.13 mmol Trolox equivalent/L and 1.01±0.09 mmol Trolox equivalent/L, respectively (p = 0.039). Mean plasma TOS levels were 28.6±7.9 µmol H 2 O 2 equivalent/L and 18.5±6.3 µmol H 2 O 2 equivalent/L, respectively (p < 0.001). Mean OSI levels were 3.08±0.98 arbitrary units and 1.84±0.64 arbitrary units, respectively (p < 0.001). A small amount of cigarette smoke (five to 10 cigarettes per day) causes considerable oxidative stress. There were significant correlations between number of cigarettes consumed and oxidant status and OSI levels. Conclusions:Passive smoke is a potent oxidant in preschool children. Its deleterious effects are not limited just to heavy passive smoking, but also occur with exposure to small amounts of smoke.J Pediatr (Rio J). 2011;87(6):523-8: Antioxidants, cotinine, oxidants, passive smoking, preschool children. ResumoObjetivos: Estudar o efeito do fumo passivo sobre o estado plasmático oxidativo e antioxidativo em pré-escolares fumantes passivos e compará-los com controles. Métodos:Trinta e quatro pré-escolares fumantes passivos (cinco a 50 cigarros/dia) (grupo de estudo) e 32 controles que nunca estiveram expostos à fumaça de cigarro foram escolhidos aleatoriamente entre crianças de 4 a 6 anos. Foram determinados os níveis de cotinina uriná-ria e de indicadores do estado oxidativo e antioxidativo, isto é, estado oxidante total (EOT), capacidade antioxidante total (CAT) e índice de estresse oxidativo (IEO). Resultados:A média do consumo ambiental de cigarros foi de 22±13 cigarros por dia nas crianças fumantes passivas. Os níveis médios de cotinina urinária foram 77,6±41,4 ng/mL e 11,9±2,3 ng/mL nos grupos de estudo e controle, respectivamente (p < 0,001). Os níveis médios da CAT plasmática foram 0,95±0,13 mmol equivalente de Trolox/L e 1,01±0,09 mmol equivalente de Trolox/L, respectivamente (p = 0,039). Os níveis médios de EOT plasmático foram 28,6±7,9 µmol H 2 O 2 equivalente/L e 18,5±6,3 µmol H 2 O 2 equivalente/L, respectivamente (p < 0,001). Os níveis médios de IEO foram 3,08±0,98 unidade arbitrária e 1,84±0,64 unidade arbitrária, respectivamente (p < 0,001). Uma pequena quantidade de fumaça de cigarro (cinco a 10 cigarros/dia) c...

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Section: Resultsunclassified

Increased oxidative stress in preschool children exposed to passive smoking

et al. 2011

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“…Moreover, autooxidation of polyhydroxyaromatic compounds such as catechol and 1,4-hydroquinone present in cigarette tar (particulate phase) has been demonstrated to induce superoxide production in lung tissue that in turn could react with ⅐ NO from the gas phase of cigarette smoke to form ONOO Ϫ . 28 ONOO Ϫ has been associated with increased oxidative reactions 29 and DNA damage, 30 and it may cause a reduction of plasma antioxidants as well. Nitration of tyrosine residues of proteins leads to the production of 3-nitrotyrosine that may be considered as a marker of ONOO Ϫ -dependent oxidative damage.…”

Section: Discussionmentioning

confidence: 99%

Tetrahydrobiopterin Improves Endothelium-Dependent Vasodilation in Chronic Smokers

Heitzer

Brockhoff

Mayer

et al. 2000

Circulation Research

407

278

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Abstract-Conditions associated with impaired nitric oxide (NO) activity and accelerated atherosclerosis have been shown to be associated with a reduced bioavailability of tetrahydrobiopterin (BH4). We therefore hypothesized that BH4 supplementation may improve endothelial dysfunction of chronic smokers. Forearm blood flow (FBF) responses to the endothelium-dependent vasodilators acetylcholine (ACh; 0.75, 1.5, and 3.0 g/100 mL tissue/min) or serotonin (5-HT; 0.7, 2.1, and 6.3 ng/100 mL tissue/min), to the inhibitor of endothelial nitric oxide synthase (NOS) N G -monomethyl-L-arginine (L-NMMA; 2, 4, and 8 mol/min), and to the endothelium-independent vasodilator sodium nitroprusside (SNP; 0.1, 0.3, and 1.0 g/100 mL tissue/min) were measured by venous occlusion plethysmography in controls and chronic smokers. Drugs were infused into the brachial artery, and FBF was measured before and during concomitant intra-arterial infusion of BH4, tetrahydroneopterin (NH4; another reduced pteridine), or the antioxidant vitamin C (6 and 18 mg/min). In control subjects, BH4 had no effect on FBF in response to ACh, 5-HT, and SNP. In contrast, in chronic smokers, the attenuated FBF responses to ACh and 5-HT were markedly improved by concomitant administration of BH4, whereas the vasodilator responses to SNP were not affected. L-NMMA-induced vasoconstriction was significantly reduced in smokers compared with controls, suggesting impaired basal NO bioactivity. BH4 improved L-NMMA responses in smokers while having no effect on L-NMMA responses in controls. Pretreatment with vitamin C abolished BH4 effects on ACh-dependent vasodilation. In vitro, NH4 scavenged superoxide created by the xanthine/xanthine oxidase reaction equipotent like BH4 but failed to modify ACh-induced changes in FBF in chronic smokers in vivo. These data support the concept that in addition to the free radical burden of cigarette smoke, a dysfunctional NOS III due to BH4 depletion may contribute at least in part to endothelial dysfunction in chronic smokers. The full text of this article is available at http://www.circresaha.org. (Circ Res. 2000;86:e36-e41.)

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“…If it is reasonable to invoke the higher levels of gonadotropins to explain the effects of carotene on postmenopausal disease, then estrogen could be a factor mediating the effects of lycopene on premenopausal disease. Here, we should consider the possibility that the pro-oxidant and potentially DNAdamaging activity of catechol estrogens, 40 which would be higher in premenopausal women, could be countered by the strong freeradical scavenging activity of lycopene. Our exercise in constructing biologic plausibility is incomplete without a discussion of the factors that could affect the validity of our findings, including the inability to assess long-term diet and possibilities for recall bias, selection bias or confounding.…”

Section: Discussionmentioning

confidence: 99%

Carotenoids, antioxidants and ovarian cancer risk in pre- and postmenopausal women

Cramer¹,

Kuper²,

Harlow³

et al. 2001

Int. J. Cancer

106

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An inverse association between ovarian cancer risk, carotenoids and antioxidant vitamins has been suggested by several epidemiologic studies and 1 experimental trial of a vitamin A analogue. From a population-based study of 549 cases of ovarian cancer and 516 controls, we estimated the consumption of the antioxidant vitamins A, C, D and E and various carotenoids, including alpha-and beta-carotene and lycopene, using a validated dietary questionnaire. Multivariate logistic regression was used to calculate the exposure odds ratios adjusted for established ovarian cancer risk factors. Intakes of carotene, especially alpha-carotene, from food and supplements were significantly and inversely associated with risk for ovarian cancer, predominantly in postmenopausal women. Intake of lycopene was significantly and inversely associated with risk for ovarian cancer, predominantly in premenopausal women. Food items most strongly related to decreased risk for ovarian cancer were raw carrots and tomato sauce. Carotenoids include substances able to be converted into vitamin A, such as alpha-and beta-carotene, as well as other compounds, which cannot be converted into vitamin A but have more potent antioxidant properties, such as lycopene from tomatoes. Together with vitamins A, C and E, the carotenoids are believed to be important in cancer prevention because of their properties as antioxidants or their ability to affect cell differentiation or proliferation. Whether these substances affect risk for ovarian cancer is of interest given its high case-fatality ratio. Three case-control studies have reported that either beta-carotene or vitamin A might be inversely related to ovarian cancer risk. [1][2][3] In addition, an experimental trial to assess whether the vitamin A analogue, fenretinide, might prevent a second breast cancer yielded the surprising finding of a decreased risk for ovarian cancer. 4 In our report, we assessed the association between ovarian cancer and vitamins A, C, E and the carotenoids using data from a population-based case-control study. Taking the lead from an investigation of breast cancer suggesting that menopausal status might modify the association between carotenoids and breast cancer risk, 5 we examined whether menopausal status also influenced associations with ovarian cancer. MATERIAL AND METHODSThe parent study has been described previously. 6 Briefly, between May 1992 and March 1997, 1,080 incident cases of ovarian cancer among women residing in eastern Massachusetts or New Hampshire were identified through hospital tumor boards and statewide cancer registries. We excluded 203 of these cases because they had died (n ϭ 91), moved or had no phone (n ϭ 51), did not speak English (n ϭ 14) or had a nonovarian primary on review (n ϭ 47); 877 eligible women remained. Physicians denied access to 126 (14%) of these women, 136 (16%) declined to participate and 52 (6%) cases with nonepithelial tumors were excluded, leaving 563 cases with epithelial ovarian cancer, including tumors of borderline malignancy, ...

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Synergistic induction of DNA strand breakage by cigarette tar and nitric oxide

Cited by 77 publications

References 4 publications

Increased oxidative stress in preschool children exposed to passive smoking

Increased oxidative stress in preschool children exposed to passive smoking

Tetrahydrobiopterin Improves Endothelium-Dependent Vasodilation in Chronic Smokers

Carotenoids, antioxidants and ovarian cancer risk in pre- and postmenopausal women

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