Role of oxygen free radicals in the induction of sister chromatid exchanges by cigarette smoke

Lee, Chin K.; Brown, Buddy G.; Rice, William Y.; Doolittle, David J.

doi:10.1002/em.2850130107

Cited by 17 publications

(6 citation statements)

References 17 publications

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“…This in vivo induction may be primarily caused by pathways not involving free radicals or oxidation reactions. This possibility is supported by in vitro experiments on SCE induction by cigarette smoke (Lee et al, 1989). If so, this would explain the absence of an effect of p-carotene without precluding its protective potential in other DNAdamaging pathways.…”

Section: Discussionmentioning

confidence: 92%

No influence of beta‐carotene on smoking‐induced dna damage as reflected by sister chromatid exchanges

Poppel

Kok

Duijzings

et al. 1992

Intl Journal of Cancer

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The putative cancer-preventive potential of beta-carotene may be explained by its anti-oxidant capacity to prevent free-radical-induced DNA damage. To evaluate this hypothesis, we studied the effect of 14 weeks of beta-carotene supplementation on the frequency of sister chromatid exchanges (SCE) in lymphocytes in 143 heavy smokers in a randomized, double-blind, placebo-controlled intervention trial. Age, smoking habits and pretreatment blood levels of cotinine, beta-carotene, retinol and vitamins C and E were similar in the placebo group (n = 73) and the treatment group (n = 70). Plasma beta-carotene levels increased 13-fold in the treatment group during intervention, whereas the other parameters remained stable in both groups. Initial SCE levels were similar in the treatment and placebo groups (5.10 +/- 0.98 vs. 5.00 +/- 0.99 SCE/lymphocyte). During the intervention, both groups showed an almost identical decrease, and at the end of the intervention period there was no difference in SCE levels between the treatment and the placebo groups (4.37 +/- 0.38 vs. 4.24 +/- 0.37 SCE/lymphocyte). This study shows no protective effect of beta-carotene on DNA damage as reflected by sister chromatid exchanges in lymphocytes. Our results thus do not yield support for a cancer-preventive mechanism of beta-carotene involving this form of DNA damage. It cannot be excluded, however, that beta-carotene prevents other forms of smoking-induced DNA damage, affects other tissues, or is preventive in later stages of carcinogenesis.

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Section: Discussionmentioning

confidence: 92%

No influence of beta‐carotene on smoking‐induced dna damage as reflected by sister chromatid exchanges

Poppel

Kok

Duijzings

et al. 1992

Intl Journal of Cancer

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“…Reactive oxyradicals are known mediators of the indirect effect of ionizing radiation. There is considerable evidence, including ours, that ROS are involved in the genotoxicity of arsenite (22,53), asbestos (38,54), and cigarette smoke condensate (55). With the use of Chinese hamster ovary cells and an x-ray-hypersensitive, DNA repair-deficient mutant, XRS-5, Wang and Huang showed that arsenite induced a dosedependent increase in micronuclei that was blocked by exogenous catalase (41).…”

Section: Discussionmentioning

confidence: 98%

Induction of oxyradicals by arsenic: Implication for mechanism of genotoxicity

Liu

Athar

Lippai

et al. 2001

Proc. Natl. Acad. Sci. U.S.A.

432

192

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Although arsenic is a well-established human carcinogen, the mechanisms by which it induces cancer remain poorly understood. We previously showed arsenite to be a potent mutagen in humanhamster hybrid (AL) cells, and that it induces predominantly multilocus deletions. We show here by confocal scanning microscopy with the fluorescent probe 5,6-chloromethyl-2,7-dichlorodihydrofluorescein diacetate that arsenite induces, within 5 min after treatment, a dose-dependent increase of up to 3-fold in intracellular oxyradical production. Concurrent treatment of cells with arsenite and the radical scavenger DMSO reduced the fluorescent intensity to control levels. ESR spectroscopy with 4-hydroxy-2,2,6,6-tetramethyl-1-hydroxypiperidine (TEMPOL-H) as a probe in conjunction with superoxide dismutase and catalase to quench superoxide anions and hydrogen peroxide, respectively, indicates that arsenite increases the levels of superoxide-driven hydroxyl radicals in these cells. Furthermore, reducing the intracellular levels of nonprotein sulfhydryls (mainly glutathione) in A L cells with buthionine S-R-sulfoximine increases the mutagenic potential of arsenite by more than 5-fold. The data are consistent with our previous results with the radical scavenger DMSO, which reduced the mutagenicity of arsenic in these cells, and provide convincing evidence that reactive oxygen species, particularly hydroxyl radicals, play an important causal role in the genotoxicity of arsenical compounds in mammalian cells.

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“…The effects of cigarette smoke on oxidative stress are well known as are the effects of smoke on cellular apoptosis [59]–[61]. Increased lipid peroxidation, reduced glutathione contents, increased catalase activity, decreased SOD activity, cytoplasmic retractions and fewer intercellular junctions were observed in granulosa cells exposed to Cd [62], [63], a heavy metal compound in cigarette smoke.…”

Section: Discussionmentioning

confidence: 99%

The Effects of Cigarette Smoke Extract on Ovulation, Oocyte Morphology and Ovarian Gene Expression in Mice

Mai

Lei

et al. 2014

PLoS ONE

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Cigarette smoking can harm fertility, but the existing research has targeted primarily on ovarian follicles, embryos or sex hormone. In this study, we tested cigarette smoke extract on ovulation, oocyte morphology and ovarian gene expression associated with inhibition of oxidative stress using C57BL/6 mice. Mice in the experimental group were administered a cigarette smoke extract (CSE) solution (2 mg/ml) orally daily, while the blank control group was given dimethylsulfoxide (DMSO). A positive control group (menadione) was used that received an intraperitoneal injection of 15 mg/kg menadione in oil solution daily. We found that the CSE group manifested a reduced diameter of zona pellucida-free oocyte (ZP-free OD) and a morphologically misshapen first polar body (PB). Our results suggest that CSE exposure is associated with a shrink size and poor quality of oocytes. Quitting smoking is a wise choice to ensure good fertility.

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Role of oxygen free radicals in the induction of sister chromatid exchanges by cigarette smoke

Cited by 17 publications

References 17 publications

No influence of beta‐carotene on smoking‐induced dna damage as reflected by sister chromatid exchanges

No influence of beta‐carotene on smoking‐induced dna damage as reflected by sister chromatid exchanges

Induction of oxyradicals by arsenic: Implication for mechanism of genotoxicity

The Effects of Cigarette Smoke Extract on Ovulation, Oocyte Morphology and Ovarian Gene Expression in Mice

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