Genotoxicity of tobacco smoke and tobacco smoke condensate: a review

DeMarini, David M.

doi:10.1016/j.mrrev.2004.02.001

Cited by 434 publications

(293 citation statements)

References 319 publications

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“…1, only the high dose of MTS produced slight, but statistically significant, increases in the frequencies of MN-RETs (0.68% vs. 0.52% in controls; P = 0.03, unadjusted) and MN-NCEs (0.16% vs. 0.15% in controls; P = 0.04, unadjusted). These results confirm that MTS induces MN in the hematopoietic system, as previously shown (3,24). Conversely, neither dose of STS significantly increased the frequencies of MN-RETs or MN-NCEs with respect to control values in bone marrow and blood, respectively (using a generalized score test or ANOVA).…”

Section: Resultssupporting

confidence: 89%

Sidestream tobacco smoke is a male germ cell mutagen

Marchetti

Rowan-Carroll

Williams

et al. 2011

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

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Active cigarette smoking increases oxidative damage, DNA adducts, DNA strand breaks, chromosomal aberrations, and heritable mutations in sperm. However, little is known regarding the effects of second-hand smoke on the male germ line. We show here that short-term exposure to mainstream tobacco smoke or sidestream tobacco smoke (STS), the main component of secondhand smoke, induces mutations at an expanded simple tandem repeat locus (Ms6-hm) in mouse sperm. We further show that the response to STS is not linear and that, for both mainstream tobacco smoke and STS, doses that induced significant increases in expanded simple tandem repeat mutations in sperm did not increase the frequencies of micronucleated reticulocytes and erythrocytes in the bone marrow and blood of exposed mice. These data show that passive exposure to cigarette smoke can cause tandem repeat mutations in sperm under conditions that may not induce genetic damage in somatic cells. Although the relationship between noncoding tandem repeat instability and mutations in functional regions of the genome is unclear, our data suggest that paternal exposure to second-hand smoke may have reproductive consequences that go beyond the passive smoker.DNA mutation | micronuclei | germline | spermatogenesis D espite years of intense public campaigns to limit and reduce tobacco consumption, smoking is still widespread, and its health effects remain a significant public concern. Approximately 35% of men of reproductive age in the United States smoke cigarettes (1), and there is extensive evidence to suggest that tobacco smoking can result in abnormal reproductive outcomes such as spontaneous abortions and birth defects (2). Men who smoke are at high risk for several semen abnormalities, including reduced motility, sperm DNA damage such as DNA breaks and adducts, and chromosomal abnormalities (3). In mice, exposure to mainstream tobacco smoke (MTS) induces germ-line mutations in expanded simple tandem repeats (ESTR) that can be transmitted to the progeny, causing irreversible modifications in the genome of the offspring (4). Recently, the International Agency for Research on Cancer concluded that there is enough evidence to link paternal smoking in humans with increased risk of childhood cancer, suggesting that tobacco smoking causes heritable germ cell mutation in humans (5).Exposure to second-hand smoke also remains widespread, with an estimated 40% of nonsmokers being exposed to secondhand smoke (6). Much less is known about the health effects of second-hand (or passive) smoking, although evidence is rapidly accumulating that exposure to second-hand smoke can be as harmful and hazardous to human health as active smoking (6, 7), and that there may be no risk-free level of exposure (8). Sidestream tobacco smoke (STS), the main component of secondhand smoke, is a complex mixture of more than 4,000 chemicals, including at least 50 known carcinogens (8). Qualitative differences between MTS-the smoke inhaled by active smokers-and STS are small; however, some toxicants...

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Section: Resultssupporting

confidence: 89%

Sidestream tobacco smoke is a male germ cell mutagen

Marchetti

Rowan-Carroll

Williams

et al. 2011

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

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“…It is known that smokers have higher levels of DNA damage in their sperm. 16 In this context, the presence of the GSTP1 enzyme in seminal fluid further substantiates its role in the protection of spermatozoa against (oxidative) damage. 40 However, our results did not reveal a significant association between the paternal GSTP1 Val105 allele, alone or in combination with paternal smoking and CL/P offspring.…”

Section: Discussionmentioning

confidence: 79%

“…However, the genetic background of the child is derived from both parents, whose gametes may be affected by lifestyle factors. 15 Therefore, paternal lifestyle factors, such as smoking, may generate cytotoxic effects 16 and could as such contribute to orofacial clefts in newborns.…”

Section: Introductionmentioning

confidence: 99%

The I105V polymorphism in glutathione S-transferase P1, parental smoking and the risk for nonsyndromic cleft lip with or without cleft palate

et al. 2008

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Genetic variations in the detoxification enzyme glutathione S-transferase P1 (GSTP1) may modify the teratogenicity of lifestyles, such as smoking. We investigated the role of the I105V polymorphism in GSTP1, parental periconception smoking, and their interaction with nonsyndromic cleft lip with or without cleft palate (CL/P) risk in the offspring. The GSTP1 I105V polymorphisms were determined in Dutch nonconsanguineous Caucasians comprising of 155 CL/P triads (mother, father, child) and 195 control triads. The analyses were also carried out on complete triads only (n ¼ 69 CL/P and n ¼ 95 controls). Transmission disequilibrium testing and logistic regression analyses were performed. Neither maternal nor paternal smoking increased CL/P risk; odds ratios (OR): 1.2, 95 confidence intervals (CI) ¼ 0.7-2.0 and OR: 1.0, 95% CI ¼ 0.6-1.6, respectively. Carriership of the polymorphic Val105 allele in mothers may increase CL/P risk, OR: 1.5, 95% CI ¼ 0.96-2.5. Children homozygous for the Val105 allele may show an increased risk of CL/P, OR: 2.2, 95% CI ¼ 0.8-6.4. Maternal smoking tended to increase CL/P risk in mothers and children carrying Val105 alleles, OR ¼ 1.9, 95% CI ¼ 0.9-4.0 and OR ¼ 2.2, 95% CI ¼ 0.98-4.9, respectively. The highest risk for CL/P in children carrying Val105 alleles with a smoking father was 1.7, 95% CI ¼ 0.8-3.5. The GSTP1 I105V polymorphism in mothers and/or children either alone or in combination with maternal smoking may contribute to CL/P risk. Although of borderline significance, these results may underline the importance of smoking cessation in the periconception period for the prevention of CL/P in future generations.

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“…Three recent studies have provided evidence that this could be the case (Hong et al, 2005;Zhang et al, 2006;Dharel et al, 2006). DNA damage is just one form of genotoxic stress that cells undergo when exposed to smoke (DeMarini, 2004). Two recent papers from the Chinese Academy of Medical Sciences suggest that smoking and a inherently weaker p53 stress response, interact to increase the risk for developing both lung and esophageal cancers (Hong et al, 2005;Zhang et al, 2006).…”

Section: Stresses Such As Smoking and Chronic Hcv Infectionmentioning

confidence: 99%

A single nucleotide polymorphism in the p53 pathway interacts with gender, environmental stresses and tumor genetics to influence cancer in humans

2007

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Cancer biology finds itself in a post-genomic era and the hopes of using inherited genetic variants to improve prevention and treatment strategies are widespread. One of the largest types of inherited genetic variation is the single nucleotide polymorphism (SNP), of which there are at least 4.5 million. The challenge now becomes how to discover which polymorphisms alter cancer in humans and how to begin to understand their mechanism of action. In this report, a series of recent publications will be reviewed that have studied a polymorphism in the p53 tumor suppressor pathway, MDM2 SNP309. These reports have lent insights into how germline genetic variants of the p53 pathway could interact with gender, environmental stresses and tumor genetics to affect cancer in humans. Importantly, these observations have also exposed potential nodes of intervention, which could prove valuable in both the prevention and treatment of this disease in humans.

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Genotoxicity of tobacco smoke and tobacco smoke condensate: a review

Cited by 434 publications

References 319 publications

Sidestream tobacco smoke is a male germ cell mutagen

Sidestream tobacco smoke is a male germ cell mutagen

The I105V polymorphism in glutathione S-transferase P1, parental smoking and the risk for nonsyndromic cleft lip with or without cleft palate

A single nucleotide polymorphism in the p53 pathway interacts with gender, environmental stresses and tumor genetics to influence cancer in humans

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