The association between genetic damage in peripheral blood lymphocytes and polymorphisms of three glutathione S-transferases in Chinese workers exposed to 1,3-butadiene

Cheng, Xuemei; Zhang, Tianliang; Zhao, Jingping; Zhou, Jingyang; Shao, Hua; Zhou, Zhonghua; Kong, Fanling; Feng, Na; Sun, Yuan; Shan, Bao-de; Zhang, Xia

doi:10.1016/j.mrgentox.2012.10.008

Cited by 16 publications

(11 citation statements)

References 28 publications

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“…Several works have studied the effect of sex on DNA damage. Despite the fact that some studies have identified differences between sexes in DNA damage [23, 26, 36], our results based on analysis of 36 studies have shown no such differences. This means that both sexes show increased DNA damage with age, even though the absolute values could be different.…”

Section: Discussioncontrasting

confidence: 96%

Aging and DNA damage in humans: a meta-analysis study

Soares

Cortinhas

Bento

et al. 2014

Aging

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Age-related DNA damage is regarded as one of the possible explanations of aging. Although a generalized idea about the accumulation of DNA damage with age exists, results found in the literature are inconsistent. To better understand the question of age-related DNA damage in humans and to identify possible moderator variables, a meta-analysis was conducted.Electronic databases and bibliographies for studies published since 2004 were searched. Summary odds ratios (ORs) and 95% confidence intervals (CIs) for age-related DNA damage were calculated in a random-effects model.A total of 76 correlations from 36 studies with 4676 participants were included. Based on our analysis, a correlation between age and DNA damage was found (r = 0.230, p = 0.000; 95% confidence interval = 0.111 - 0.342). The test for heterogeneity of variance indicates that the study´s results are significantly high (Q (75) = 1754.831, p = 0.000). Moderator variables such as smoking habits, technique used, and the tissue/sample analyzed, are shown to influence age-related DNA damage (p=0.026; p=0.000; p=0.000, respectively). Nevertheless, sex did not show any influence on this relation (p=0.114).In conclusion, this meta-analysis showed an association between age and DNA damage in humans. It was also found that smoking habits, the technique used, and tissue/sample analyzed, are important moderator variables in age-related DNA damage.

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Section: Discussioncontrasting

confidence: 96%

Aging and DNA damage in humans: a meta-analysis study

Soares

Cortinhas

Bento

et al. 2014

Aging

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“…It has been speculated that there may be other sources of DHBMA exposure that have not yet been identified(44). A study among Chinese rubber factory workers found that DHBMA levels correlated with airborne BD levels(25). In our stepwise regression analyses we did find that daily alcohol consumption (g/1000kcal/day) was positively associated with DHBMA levels.…”

Section: Discussionmentioning

confidence: 99%

“…Studies have found that the distribution of functional genetic variants in BD metabolizing genes, such as EH , CYP2A6 , CYP2E1 and GSTT1 , substantially differs by racial/ethnic groups (20–24). The GSTT1 -null genotype has been reported to be associated with a frequency of BD exposure-induced chromosomal damage(24, 25). Therefore, inter-ethnic and inter-individual differences in the frequency of polymorphisms in genes influencing BD metabolism could lead to higher concentration of carcinogenic epoxides in certain individuals/groups.…”

Section: Introductionmentioning

confidence: 99%

1,3-Butadiene Exposure and Metabolism among Japanese American, Native Hawaiian, and White Smokers

Park

Kotapati

Wilkens

et al. 2014

Cancer Epidemiology, Biomarkers &Amp; Prevention

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Background We hypothesize that the differences in lung cancer risk in Native Hawaiians (NH), whites and Japanese Americans (JA), may in part be due to variation in the metabolism of 1,3-butadiene (BD), one of the most abundant carcinogens in cigarette smoke. Methods We measured two biomarkers of BD exposure, monohydroxybutyl mercapturic acid (MHBMA) and dihydroxybutyl mercapturic acid (DHBMA) in overnight urine samples among 585 NH, JA and white smokers in Hawaii. These values were normalized to creatinine levels. Ethnic-specific geometric means were compared adjusting for age at urine collection, sex, body mass index and nicotine equivalents (a marker of total nicotine uptake). Results We found that mean urinary MHBMA differed by race/ethnicity (p=0.0002). The values were highest in whites and lowest in JA. This difference was only observed in individuals with the GSTT1-null genotype (p=0.0001). No difference across race/ethnicity was found among those with at least one copy of the GSTT1 gene (p≥0.72). Mean urinary DHBMA did not differ across racial/ethnic groups. Conclusions The difference in urinary MHBMA excretion levels from cigarette smoking across three ethnic groups is in part explained by the GSTT1 genotype. Mean urinary MHBMA levels are higher in whites among GSTT1-null smokers. Impact The overall higher excretion levels of MHBMA in whites and lower levels of MHBMA in JA are consistent with the higher lung cancer risk in the former. However, the excretion levels of MHBMA in NH are not consistent with and, thus, unlikely to explain, their high risk of lung cancer.

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“…The GSTM1 and GSTT1 genetic polymorphisms were evaluated using the PCR technique as described by Singh et al (2011) and Cheng et al (2013). Primers for GSTM1 were F:5-GAACTCCCTGAAAAGCTAAAGC-3, and R:5-GTTGGGCTCAAATATACGGTGG-3, and those for GSTT1 were F:5-TTCCTTACTGGTCCTCACATCTC-3 and R:5-TCACCGGATCATGGCCAGCA-3.…”

Section: Methodsmentioning

confidence: 99%

“…Experiments were repeated at least twice using both of the standard genotyping protocols. Detection of the GSTP1 codon 105 Ile to Val polymorphism (Ile105val, rs1695) was performed by PCR–RFLP technique, as described previously (Cheng et al 2013). DNA templates were amplified with the primers: 5-CTTCCACGCACATCCTCTTCC-3 (upstream) and 5-AAGCCCCTTTCTTT TTCAGC-3 (downstream).…”

Section: Methodsmentioning

confidence: 99%

Association between polymorphism of GSTP1, GSTT1, GSTM1 and CYP2E1 genes and susceptibility to benzene-induced hematotoxicity

et al. 2017

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Occupational exposure to benzene has been associated with leukemia, anemia, leukopenia, and thrombocytopenia. Genetic susceptibility to benzene toxicity in humans may be related to variations in benzene metabolizing genes. The main objective of this study was to ascertain whether polymorphism of GSTP1, GSTM1, GSTT1 and CYP2E1 genes might influence susceptibility to the adverse effects of benzene among employees of a petrochemical plant. In this cross-sectional study, 124 employees of a petrochemical plant who had been occupationally exposed to benzene and had one or more abnormal hematological parameter (cases) and 184 subjects with a similar exposure scenario, free from any abnormal hematological parameters (referent) were studied. Atmospheric concentrations of benzene were measured and GSTM1 and GSTT1 genotypes were evaluated using the multiplex polymerase chain reaction (PCR) technique. Additionally, GSTP1 and CYP2E1 genotypes were determined by PCR- restriction fragment length polymorphism (PCR–RFLP). The frequency of null GSTT1 genotype in cases was significantly higher than that of referent group (32.3 vs. 18.5%, OR 2.1, 95% CI 1.23–3.56, p = 0.004). The mean value of platelets in subjects with null GSTT1 genotype was significantly lower than that of individuals with positive GSTT1 genotype (p = 0.015). Conversely, the mean value of leukocytes was significantly higher in subjects with null GSTM1 genotype as compared to those with positive GSTM1 genotype (p = 0.026). Logistic regression analysis showed that, subjects with null GSTT1 genotype had a significantly higher risk for hematological disorders, as compared to those with positive GSTT1 genotype (OR 2.1, 95% CI 1.23–3.56). Moreover, subjects with both null GSTT1 and GSTM1 genotypes had a significantly higher risk for hematological disorders as compared to subjects with positive GSTT1 and GSTM1 genotypes (OR 2.35, 95% CI 1.14–4.8). The results of this study showed that, individuals carrying null GSTT1 or both null STT1 and GSTM1 genotypes had a higher risk and were more susceptible to benzene-induced hematological disorders.

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The association between genetic damage in peripheral blood lymphocytes and polymorphisms of three glutathione S-transferases in Chinese workers exposed to 1,3-butadiene

Cited by 16 publications

References 28 publications

Aging and DNA damage in humans: a meta-analysis study

Aging and DNA damage in humans: a meta-analysis study

1,3-Butadiene Exposure and Metabolism among Japanese American, Native Hawaiian, and White Smokers

Association between polymorphism of GSTP1, GSTT1, GSTM1 and CYP2E1 genes and susceptibility to benzene-induced hematotoxicity

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