Rapid and intermediate N-acetylators are less susceptible to oxidative damage among 4,4′-methylenebis(2-chloroaniline) (MBOCA)-exposed workers

Objectives

In this study, we explored the association between a marker of oxidative stress, 8-hydroxydeoxyguanosine (8-OHdG), and genetic polymorphism of the carcinogen-metabolizing enzyme N-acetyltransferase 2 (NAT2) among 4,4′-methylenebis(2-chloroaniline) (MBOCA)-exposed workers.

Methods

The study population was recruited from four MBOCA-producing factories, and included 57 MBOCA-exposed workers and 101 unexposed control workers. Personal characteristics were collected by questionnaire. Plasma 8-OHdG levels were measured by LC/MS/MS. NAT2 alleles were measured by polymerase chain reaction-based restriction fragment length polymorphism (PCR-RFLP).

Results

NAT2 polymorphism influenced the plasma 8-OHdG levels of MBOCA-exposed workers, but not of non-exposed workers. No difference between exposed and control groups was found for the crude 8-OHdG levels among rapid, intermediate, and slow acetylators. After adjusting for gender, age, smoking, and alcohol consumption habit, the 8-OHdG concentration in the MBOCA-exposed workers was 0.18 pg/ml (95% CI −1.80 to −0.12) lower than the control group among rapid and intermediate acetylators. However, the difference between exposed and control groups was not significant for slow acetylators.

Conclusion

Gene–environment interactions could play a role in the carcinogenesis of occupational MBOCA exposure. We suggest that the impact of the NAT2 acetylator status is low, if at all, on the generation of the oxidative stress marker 8-OHdG in the investigated exposed group.     

Chromium (VI) induced oxidative damage to DNA: increase of urinary 8-hydroxydeoxyguanosine concentrations (8-OHdG) among electroplating workers

Aims: To investigate the concentration of urinary 8-hydroxydeoxyguanosine (8-OHdG) among electroplating workers in Taiwan.

Methods: Fifty workers were selected from five chromium (Cr) electroplating plants in central Taiwan. The 20 control subjects were office workers with no previous exposure to Cr. Urinary 8-OHdG concentrations were determined using high performance liquid chromatography with electrochemical detection.

Results: Urinary 8-OHdG concentrations among Cr workers (1149.5 pmol/kg/day) were higher than those in the control group (730.2 pmol/kg/day). There was a positive correlation between urinary 8-OHdG concentrations and urinary Cr concentration (r = 0.447, p < 0.01), and urinary 8-OHdG correlated positively with airborne Cr concentration (r = 0.285). Using multiple regression analysis, the factors that affected urinary 8-OHdG concentrations were alcohol, the common cold, and high urinary Cr concentration. There was a high correlation of urinary 8-OHdG with both smoking and drinking, but multiple regression analysis showed that smoking was not a significant factor. Age and gender were also non-significant factors.

Conclusion: 8-OHdG, which is an indicator of oxidative DNA damage, was a sensitive biomarker for Cr exposure.

     

Leukocyte 8-hydroxydeoxyguanosine and aromatic DNA adduct in coke-oven workers with polycyclic aromatic hydrocarbon exposure

Objective To investigate the potential for exposure to polycyclic aromatic hydrocarbons (PAHs) to induce oxidative DNA damage, we conducted a cross-sectional study in coke-oven workers employed at an iron–steel factory.Methods The study population contained 119 coke-oven workers from different work areas of the oven and 38 controls. Personal information on age, employment duration, smoking habit and alcohol consumption was obtained at an interview. Leukocyte 8-hydroxydeoxyguanosine (8-OHdG) was measured by high performance liquid chromatography with electrochemical detection. Leukocyte aromatic DNA adducts as effective dose, and urinary 1-hydroxypyren as internal dose, were also measured, and used to analyze the relationship of 8-OHdG with other biomarkers for PAH exposure, tobacco smoke and alcohol consumption.Results The leukocyte 8-OHdG revealed a wide inter-individual variation. The highest 8-OHdG level was detected in bottom-workers of the coke-oven. There were significant differences among the four different work areas (P=0.02). We could not find significant correlation between 8-OHdG levels and urinary 1-hydroxypyrene, but a weakly positive correlation was found between 8-OHdG and leukocyte aromatic DNA adducts among all subjects (r=0.19 P=0.03). We could not observe any effect of smoking and alcohol drinking on 8-OHdG production.Conclusion We could not find clear evidence that PAH exposure induces oxidative DNA damage.     

Urinary 8-hydroxy-2'-deoxyguanosine as a biomarker of oxidative DNA damage in workers exposed to fine particulates

Residual oil fly ash (ROFA) is a chemically complex mixture of compounds, including metals that are potentially carcinogenic because of their ability to cause oxidative injury. In this study, we investigated the association between exposure to particulate matter with an aerodynamic mass median diameter 相似文献   

焦炉工人血清谷胱甘肽硫转移酶活力和尿8-羟基脱氧鸟苷水平

目的 探讨血清谷胱甘肽硫转移酶（GST）和尿8-羟基脱氧鸟苷（8-OHdG）作为焦炉工人多环芳烃（PAHs）暴露生物监测标志的可行性.方法 用高效液相色谱-电化学方法和试剂盒分别检测47名男性焦炉工和31名男性对照者尿8-OHdG水平和血清GST活力;尿1-羟基芘（1-OHP）作为PAHs接触的内暴露标志,采用碱水解-高效液相色谱方法分析.结果 焦炉工人尿1-OHP浓度的中位数（P25～P75）为[5.7（1.4～12.0）μmol/mol Cr],血清GST活力为[22.1（14.9～31.2）U/ml],尿8-O-HdG水平为[1.9（1.4～15.4）μmol/mol Cr],均高于对照组工人[3.0（0.5～6.4）μmol/mol Cr、13.1（9.5～16.7）U/ml、1.3（1.0～4.0）μmol/mol Cr],差异均有统计学意义（P＜0.05或P＜0.01）.以吸烟分层,两组工人尿1-OHP浓度和血清GST活力仅在吸烟者中、尿8-OHdG水平仅在非吸烟者中差异有统计学意义（均P＜0.01）.焦炉工人血清GST活力和尿1-OHP浓度呈正相关（rs=0.31,P＜0.01,n=78）.多元Logistic回归分析显示,与对照工人相比,焦炉工人血清GST活力＞16.7 U/ml和尿8-OHdG水平＞1.8 μmol/mol Cr的OR值分别为13.2和4.4;高体重指数是影响尿8-OHdG水平下降的独立因素.结论 焦炉工人血清GST活力增强和氧化性DNA损伤增加,吸烟和职业暴露有交互作用;血清GST有可能作为PAHs暴露评价的生物标志;尿8-OHdG检测有助于焦炉工肺癌危险度评价.     

Increased levels of 8-hydroxy-2 -deoxyguanosine attributable to carcinogenic metal exposure among schoolchildren

Arsenic, chromium, and nickel are reported in several epidemiologic studies to be associated with lung cancer. However, the health effects of arsenic, chromium, and nickel exposures are equivocal for children. Therefore, we performed a cross-sectional study to investigate possible associations between the internal concentrations of arsenic, chromium, and nickel and the level of oxidative stress to DNA in children. We measured urinary levels of arsenic, chromium, and nickel for 142 nonsmoking children using atomic absorption spectrometry. As a biomarker for oxidative stress, urinary 8-hydroxy-2 -deoxyguanosine (8-OHdG) levels were analyzed with an enzyme-linked immunosorbent assay kit. The median urinary 8-OHdG level for our subjects was 11.7 ng/mg creatinine. No obvious relationship between the levels of urinary nickel and 8-OHdG was found. Multiple linear regression analysis showed that children with higher urinary chromium had greater urinary 8-OHdG than did those with lower urinary chromium. Similarly, subjects with higher urinary arsenic had greater urinary 8-OHdG than did those with lower urinary arsenic. Furthermore, children with both high urinary arsenic and high urinary chromium had the highest 8-OHdG levels (mean +/- SE, 16.0 +/- 1.3; vs. low arsenic/low chromium, p < 0.01) in urine, followed by those with low arsenic/high chromium (13.7 +/- 1.6; vs. low arsenic/low chromium, p = 0.25), high arsenic/low chromium (12.9 +/- 1.6 vs. low arsenic/low chromium, p = 0.52), and low arsenic/low chromium (11.5 +/- 1.3); the trend was significant (p < 0.001). Thus, environmental carcinogenic metal exposure to chromium and arsenic may play an important role in oxidative DNA damage to children.     

Urinary 8-hydroxydeoxyguanosine as a biomarker of oxidative DNA damage in workers exposed to ethylbenzene

This study assessed the relationships between ethylbenzene exposure and levels of 8-hydroxydeoxyguanosine (8-OHdG) among spray painters. Sixty-four male workers employed at a large shipyard were recruited for this investigation. Fifteen spray painters exposed to paint, together with two non-exposed groups, namely 19 sandblasting workers and 30 office staffs were selected as the subjects. Personal exposure to xylene and ethylbenzene in air were collected using diffusive samplers. Urine samples of the spray painters were collected after a month-long holiday leave and during the pre- and post-workshifts. Urine samples of sandblasting workers and office staffs were gathered after their shift. Urinary mandelic acid and methyl hippuric acid were used as biological indices of dose of ethylbenzene and xylene, respectively. Urinary 8-OHdG was used as biomarker of oxidative DNA damage. The post-workshift concentration of urinary 8-OHdG for 10 spray painters (30.3 ± 9.28 μg g(-1) creatinine) significantly exceeded that of holiday leave (7.20 ± 1.08 μg g(-1) creatinine; P = 0.001). The post-workshift concentration of urinary 8-OHdG was higher among 15 spray painters (29.0 ± 6.52 μg g(-1) creatinine) than sandblasting workers (9.14 ± 2.05 μg g(-1) creatinine; P = 0.01) and office staffs (8.35 ± 0.84 μg g(-1) creatinine; P = 0.007). A stepwise regression model revealed an 8.11 μg g(-1) creatinine increase per 1 p.p.m. increase in ethylbenzene [95% confidence interval (CI) 4.13-12.1]. A stepwise regression model revealed an increase of 6.04 μg g(-1) creatinine (95% CI 2.23-9.84) per 1 p.p.m. in ethylbenzene after adjustment of age (95% CI 2.23-9.84). This pilot study suggests that occupational exposure to paint increases oxidative DNA injury. Moreover, urinary 8-OHdG levels displayed greater DNA damage in spray painters compared to other unexposed groups and their holiday leave samples. A significant correlation was found between urinary 8-OHdG and the exposure to ethylbenzene. The ethylbenzene exposure could not explain all urinary 8-OHdG measured. Other components of paint deserve further investigation.     

8-Hydroxydeoxyguanosine in leukocyte DNA and urine of quartz-exposed workers and patients with silicosis

Objective: To examine radical-induced DNA damage and its elimination in workers exposed to quartz and in patients with silicosis, and to assess the relationship of these effects to lung function. Methods: Blood and spontaneous urine samples were obtained from active, quartz-exposed workers without silicosis (n=63), and from retired workers with silicosis (n=42). Levels of 8-hydroxydeoxyguanosine (8-OHdG) were determined in peripheral blood leukocyte DNA and urine, by the use of high-performance liquid chromatography coupled with ultra violet- (UV) and electrochemical detection. Results: No significant differences in the mean levels of 8-OHdG in leukocyte DNA and of urinary excretion of 8-OHdG were found between silicosis patients and quartz-exposed healthy workers. However, in the group of silicosis patients with increased oxidative DNA damage the urinary excretion of 8-OHdG was lower than in the corresponding group of active workers without silicosis. In the case of silicosis, urinary 8-OHdG correlated positively, and 8-OHdG in DNA correlated negatively, with forced expiratory volume in one second (FEV₁) and forced vital capacity (FVC). Healthy workers with a personally estimated high dust exposure in the workplace showed higher levels of 8-OHdG in DNA than did workers with moderate dust exposure. No association of 8-OHdG formation and/or elimination with duration of employment, field of activity, smoking or age was found. Conclusion: Our findings suggest that a less effective repair of 8-OHdG is associated with a higher degree of pulmonary airway obstruction in patients with silicosis. Received: 13 August 1999 / Accepted: 5 January 2000     

Effect of increased tea consumption on oxidative DNA damage among smokers: a randomized controlled study

Tea drinking has been associated with decreased occurrence of cancer and heart disease. One potential mechanism for these findings is the strong antioxidant effect of tea polyphenols. A phase II randomized controlled tea intervention trial was designed to study the effect of high consumption (4 cups/d) of decaffeinated green or black tea on oxidative DNA damage as measured by urinary 8-hydroxydeoxyguanosine (8-OHdG) among smokers over a 4-mo period. A total of 143 heavy smokers, aged 18-79 y, were randomized to drink either green or black tea or water. Levels of plasma and urinary catechins and urinary 8-OHdG were measured monthly. A total of 133 of 143 smokers completed the 4-mo intervention. Multiple linear regression models were used to estimate the main effects and interaction effect of green and black tea consumption on creatinine-adjusted urinary 8-OHdG, with or without adjustment for potential confounders. Plasma and urinary levels of catechins rose significantly in the green tea group compared with the other two groups. Assessment of urinary 8-OHdG after adjustment for baseline measurements and other potential confounders revealed a highly significant decrease in urinary 8-OHdG (-31%) after 4 mo of drinking decaffeinated green tea (P = 0.002). No change in urinary 8-OHdG was seen among smokers assigned to the black tea group. These data suggest that regular green tea drinking might protect smokers from oxidative damages and could reduce cancer risk or other diseases caused by free radicals associated with smoking.     

8-Hydroxy-2'-deoxyguanosine (8-OHdG) as a short-term predictor of regional and occupational health problems

Exposure to a large number of environmental toxins can induce damage to DNA and may play an important role in the pathophysiological processes of atherosclerosis. To examine the effect of some specific environmental conditions that predispose to sudden coronary atherosclerotic death on the level of 8-OHdG, urine samples were collected from cases of certain occupations and polluted regions that showed a high prevalence of premature deaths. The samples were then analyzed for 8-OHdG. Analysis of 108 cases and 45 controls showed a significant high level of 8-OHdG in relation to occupations, habits, residency and work shift. The mean +/- standard deviation (M +/- SD) for the control group was 4.5 +/- 2.3 ng 8-OHdG/mg creatinine (n = 45), compared to 9.1 +/- 3.1 ng/mg in taxi drivers (n = 9), 10 +/- 5.5 ng/mg in chemical factory workers (n = 16), 12.0 +/- 8.9 ng/mg in paint workers (n = 9), 14.6 +/- 11.1 ng/mg in gasoline station workers (n = 15), 15 +/- 6.1 ng/mg in cement factory workers (n = 12), 16.4 +/- 3.2 ng/mg in city center inhabitants (n = 18) and 18.6 +/- 3.2 ng/mg in smokers (n = 15). These conditions at least in the pilot study done by the author, showed some form of precipitation of sudden atherosclerotic coronary death. This work proved that the recently used 8-OHdG DNA damage biomarker may be an important marker of environmental conditions that are expected to have a serious long-term impact on the cardiovascular system.     

Urinary 8-hydoxydeoxyguanosine (8-OHdG) and plasma malondialdehyde (MDA) levels in Aldh2 knock-out mice under acetaldehyde exposure

To clarify the carcinogenicity of acetaldehyde when associated with ALDH (aldehyde dehydrogenase) 2 polymorphism, Aldh2 knock-out (Aldh2-/-) mice and their wild type (Aldh2+/+) mice were exposed to two different concentrations of acetaldehyde (125 ppm and 500 ppm) for two weeks. Aldh2-/- mice, which have the same genetic background as C57BL/6J (wild mice) except for the Aldh2 gene, were used as models of humans who lack ALDH2 activity. Urinary 8-hydroxydeoxyguanosine (8-OHdG) and plasma malondialdehyde (MDA) levels were measured as indicators of oxidative DNA damage and lipid peroxidation, respectively. At 125 ppm acetaldehyde exposure for 12 d, urinary 8-OHdG levels in Aldh2+/+ mice did not increase. However, urinary 8-OHdG levels in Aldh2-/- mice were slightly increased by the end of the exposure. On the other hand, plasma MDA levels did not increase in either Aldh2-/- orAldh2+/+ mice. At 500 ppm, urinary 8-OHdG levels in both Aldh2-/- and Aldh2+/+ mice significantly increased after 6 and 12 d, but there was no genetic difference. On the other hand, plasma MDA levels in Aldh2+/+ and Aldh2-/- mice did not increase at either 125 ppm or 500 ppm after two weeks of exposure. In conclusion, it is suspected that DNA was damaged by acetaldehyde inhalation, and that susceptibility to acetaldehyde varies according to Aldh2 genotype.     

Smoking modify the effects of polycyclic aromatic hydrocarbons exposure on oxidative damage to DNA in coke oven workers

Purpose

Coke oven emissions containing polycyclic aromatic hydrocarbons (PAHs) are predominant toxic constituents of particulate air pollution that have been linked to increased risk of lung cancer. Numerous epidemiological studies have suggested that oxidative DNA damage may play a pivotal role in the carcinogenic mechanism of lung cancer. Little is known about the effect of interaction between PAHs exposure and lifestyle on DNA oxidative damage.

Methods

The study population is composed by coke oven workers (365) and water treatment workers (144), and their urinary levels of four PAH metabolites and 8-hydroxydeoxyguanosine (8-OHdG) were determined. Airborne samples of exposed sites (4) and control sites (3) were collected, and eight carcinogenic PAHs were detected by high-performance liquid chromatography.

Results

The median values of the sum of eight carcinogenic PAHs and BaP in exposed sites were significantly higher than control sites (P?<?0.01). The study found that the urinary PAH metabolites were significantly elevated in coke oven workers (P?<?0.01). Multivariate logistic regression analysis revealed that the risk of high levels of urinary 8-OHdG will increase with increasing age, cigarette consumption, and levels of urinary 1-hydroxypyrene, and P for trend were all <0.05. Smoking can significantly modify the effects of urinary 1-hydroxypyrene on high concentrations urinary 8-OHdG, during co-exposure to both light or heavy smoking and high 1-hydroxypyrene levels (OR 4.28, 95% CI 1.32–13.86 and OR 5.05, 95% CI 1.63–15.67, respectively).

Conclusions

Our findings quantitatively demonstrate that workers exposed to coke oven fumes and smoking will cause more serious DNA oxidative damage.

     

０１４－２０１７年金华市居民脑血管病死亡情况分析

摘要：目的　分析２０１４－２０１７年金华市居民脑血管病死亡的流行病学特征,为制定脑血管病预防和控制措 施提供科学依据。方法　根据“浙江省慢性病监测信息管理系统” 中２０１４－２０１７ 年金华市９ 个县（市、 区）户籍死亡的监测数据,采用“浙江省死因监测数据审核软件” 分析脑血管病不同性别、城市农村、不 同年龄段及不同类型脑血管病死亡率、标化死亡率、潜在减寿年数（ＰＹＬＬ）、平均减寿年数（ＡＹＬＬ） 和 减寿率（ＰＹＬＬＲ）等。结果　２０１４－２０１７ 年金华市居民脑血管病死亡率为１２１．１４／１０ 万, 标化死亡率 １０８．８９／１０万,死亡率呈高水平稳定态势, 占全死因的１８．７４％, 居全死因第２ 位。其中男性死亡率 １２４．６７／１０万,标化死亡率１１２．８９／１０万,女性死亡率１１７．４６／１０万,标化死亡率１０５．０９／１０万,男性高于 女性,城市死亡率１０５．７８／１０ 万, 标化死亡率１１３．８３／１０ 万, 农村死亡率１２３．４９／１０ 万, 标化死亡率 １０８．３０／１０万,城市高于农村。≥６５岁老年人脑血管病死亡率高达１０００．２８／１０ 万,占全人群的８８．７８％。 脑血管病死亡以脑出血、脑血管后遗症和脑梗死为主,占全部脑血管病死亡的８６．８８％。２０１４－２０１７年脑血 管病潜在减寿７１１８４人年;以期望寿命为基准,脑血管病患者平均每人因脑血管病减寿３．０７岁;按总人口 计算,金华市居民平均每人因脑血管病损失３．７２‰生命年。结论　脑血管病是严重危害金华市居民身体健康 和生活质量的重点疾病,应进一步加强针对脑血管病行为危险因素开展行为干预,提高居民生命质量。 关键词：脑血管病;死亡率;标化死亡率;构成比;潜在减寿年数;平均减寿年数;减寿率 中图分类号：Ｒ１９５　　文献标识码：Ａ　　文章编号：１００９ ６６３９ （２０１９）０３ ０２０８ ０４     

Urinary Arsenic Speciation and its Correlation with 8-OHdG in Chinese Residents Exposed to Arsenic Through Coal Burning

In contrast to arsenicosis caused by consumption of water contaminated by naturally occurring inorganic arsenic, human exposure to this metalloid through coal burning has been rarely reported. In this study, arsenic speciation and 8-hydroxy-2′-deoxyguanosine (8-OHdG) levels in urine were determined in the Chinese residents exposed to arsenic through coal burning in Guizhou, China, an epidemic area of chronic arsenic poisoning caused by coal burning. The urinary concentrations of inorganic arsenic (iAs), monomethylarsonic acid (MMA), dimethylarsinic acid (DMA) and total arsenic (tAs) of high-arsenic exposed subjects were significantly higher than those of low-arsenic exposed residents. A biomarker of oxidative DNA damage, urinary 8-OHdG level was significantly higher in high-arsenic exposed subjects than that of low exposed. Significant positive correlations were found between 8-OHdG levels and concentrations of iAs, MMA, DMA and tAs, respectively. In addition, a significant negative correlation was observed between 8-OHdG levels and the secondary methylation ratio (DMA/(MMA + DMA)). The results suggest that chronic arsenic exposure through burning coal rich in arsenic is associated with oxidative DNA damages, and that secondary methylation capacity is potentially related to the susceptibility of individuals to oxidative DNA damage induced by arsenic exposure through coal burning in domestic living.     

复杂电磁环境工作人员尿中8-羟基脱氧鸟苷和8-羟基鸟苷水平及其影响因素分析

目的 对复杂电磁环境(complex electromagnetic environment, CEE)工作人员的DNA和RNA氧化损伤情况以及其影响因素进行分析，为预防和控制职业病危害提供科学依据。方法 采用方便抽样法选择武汉某芯片厂CEE工作人员(n=133)为暴露组和办公室人员(n=56)为对照组，用稀释法和液相色谱-三重四级杆质谱仪测量氧化应激标志物8-羟基脱氧鸟苷(8-OHdG)和8-羟基鸟苷(8-OHG)在其尿液样本中的浓度。根据问卷调查结果，用logistic回归法分析影响8-OHdG的相关因素。结果 暴露组人员尿中的8-OHdG和8-OHG,经尿比重调整后浓度中位数分别为9.34 ng/ml和17.08 ng/ml。与对照组相比，暴露组8-OHdG浓度高于对照组，且差异有统计学意义(Z=-2.194,P=0.028)。CEE(OR=3.07,95%CI:1.35～7.00)、吸烟(OR=2.62,95%CI:1.13～6.08)和运动(OR=2.5,95%CI:1.04～6.00)为危险因素；女性(OR=0.09,95%CI:0.03～0.28)为保护因素。结论 长期暴...     

烹调油烟多环芳烃暴露与职业接触人群DNA氧化性损伤

目的 通过调查不同组别厨师和非暴露组尿中8-羟基脱氧鸟苷(8-OHdG)的排泄量,研究8-OHdG和1-羟基芘(1-OHP)之间的关系.方法 采集不同组别厨师组(n=86)和非暴露对照组(n=36)的尿液样本,观察对象均为年龄22～28岁男性,并有相似的吸烟习惯.在采样之前24 h内,以问卷调查的形式对研究对象的身体健康状况、职业史、吸烟习惯和酒精消费量进行评估.冷藏尿液样本,随后通过高效液相色谱法分析8-OHdG和1-OHP水平.结果 对照组尿液中8-OHdG的排泄量(平均1.2μmo1/mol肌酐,n=36)与厨房里有排烟设备运转的厨师组相似(平均1.5 μmol/mol肌酐,n=45).与对照组相比,接触油烟而排烟设备没有运转的厨师组,其尿8-OHdG的排泄量明显增加(平均2.3 μmol/mol 肌酐,n=18).经多元回归分析,尿ln 1-OHP和ln 8-OHdG的水平仍然呈明显的正相关.结论 接触油烟中的多环芳烃(PAH)或其他化合物可能导致DNA氧化损伤.     

吸烟和年龄对电子垃圾拆解工人尿液中8-羟基脱氧鸟苷的影响

目的 研究吸烟和年龄对电子垃圾拆解工人尿液中8-羟基脱氧鸟苷(8-hydroxy-2'-deoxyguanosine,8-OHdG)的影响.方法 采用固相萃取-高效液相色谱电化学检测器(SPE-HPLC-ECD)方法,检测64名电子垃圾拆解男性工人上班前和下班后尿液中8-OHdG浓度.按照吸烟情况和工人的年龄分别对数据进行统计分析.结果 相对于吸烟者(42名),不吸烟者(22名)尿中8-OHdG浓度明显的增高,上班前,不吸烟组的工人尿液中的8-OHdG浓度为(8.25±4.23)μmol/mol肌酐,吸烟组工人尿液中8-OHdG浓度为(5.44±1.18)μmol/mol肌酐,两者差异无统计学意义(t=-0.81,P=0.42).而在下班后,不吸烟组的工人尿液中的8-OHdG浓度为(43.12±16.19)μmol/mol肌酐,大约是吸烟组工人尿液中8-OHdG浓度[(14.82±2.51)μmol/mol肌酐]的3倍.经过1 d暴露下班后,吸烟和不吸烟工人尿液中的8-OHdG浓度差异具有统计学意义(t=-2.33,P<0.05).按照工人的年龄分组,上班前,19岁～(6名)、20岁～(22名)、30岁～(23名)、40～49岁(11名)组工人尿中8-OHdG浓度分别为(1.86±0.66)、(3.57±0.54)、(8.12±4.10)、(11.39±3.70)μmol/mol肌酐,组间差异没有统计学意义(F=0.98,P=0.41);但经过1 d的暴露,下班后,19岁～、20岁～、30岁～、40～49岁组工人尿中8-OHdG浓度分别为(4.19±2.85)、(19.89±5.26)、(28.89±14.61)、(34.94±12.50)μmol/mol肌酐,组间差异具有统计学意义(F=4.81,P=0.03).结论 吸烟对拆解工人尿中8-OHdG浓度有一定的抑制作用,尿中8-OHdG浓度随年龄增高而增加.     

Lower serum levels of beta-carotene in Lithuanian men are accompanied by higher urinary excretion of the oxidative DNA adduct, 8-hydroxydeoxyguanosine. The LiVicordia study

OBJECTIVE: In 1995, middle-aged Lithuanian men had a four-fold higher risk than Swedish men of dying from coronary heart disease. The cross-sectional LiVicordia study had reported significantly lower levels of the lipid-soluble antioxidants lycopene, beta-carotene, and gamma-tocopherol among Lithuanian men than among Swedish men. We examined whether there were differences in urinary 8-hydroxydeoxyguanosine (8OHdG), a marker of oxidative stress, between these groups of men. METHODS: Using automated coupled column high-performance liquid chromatography with electrochemical detection, we examined 50-y-old men randomly sampled from Link?ping, Sweden (n = 99) and Vilnius, Lithuania (n = 109) with regard to urinary concentrations of 8-OHdG. RESULTS: Levels of 8-OHdG were higher in the Lithuanian men than in the Swedish men (20.9 +/- 0.91 versus 14.9 +/- 0.75 nM/L, P < 0.001), and this difference was evident in smokers (P < 0.01) and non-smokers (P < 0.001). Serum levels of alpha- and beta-carotene were inversely correlated to urinary 8-OHdG levels (P < 0.05 in both cases). Habitual smoking and low levels of beta-carotene contributed significantly to higher oxidative DNA damage expressed as urinary 8-OHdG. CONCLUSIONS: These findings indicate that increased urinary 8-OHdG levels accompany lower serum levels of antioxidants in Lithuanian men. They supported previous suggestions that increased oxidative stress may be one factor behind the higher mortality in Lithuanian men.     

8-Hydroxydeoxyguanosine in human leukocyte DNA and daily health practice factors: effects of individual alcohol sensitivity.

A typical oxidative DNA damage, 8-hydroxydeoxyguanosine (8-OHdG), was evaluated in human polymorphonuclear leukocytes (PMN) and mononuclear leukocytes (MN) by an anaerobic determination method. The mean 8-OHdG values were the lowest level ever reported [PMN, 3.07 +/- 1.45; MN, 2.37 +/- 1.21 8-OHdG/10(6) deoxyguanosine molecules (dG); n = 92]. According to a self-administered questionnaire to 92 healthy male workers, the relationship was investigated between 8-OHdG in leukocytes and daily health practice factors, that is, the frequency of physical exercise, smoking status, alcohol drinking, nutritional balance, and the degree of mental stress. A significant difference was observed only in alcohol drinking in subjects classified by aldehyde-dehydrogenase 2 isozyme (ALDH2) genotype. Habitual alcohol intake appeared to increase 8-OHdG in PMN from ALDH2-deficient subjects. Neither age, body mass index, nor any other factors examined showed any significant correlation with the 8-OHdG levels in leukocytes.     

Exposure to traffic exhausts and oxidative DNA damage

Aims: To assess the relations between exposure to traffic exhausts and indicators of oxidative DNA damage among highway toll station workers.

Methods: Cross-sectional study of 47 female highway toll station workers exposed to traffic exhausts and 27 female office workers as a reference group. Exposure assessment was based on average and cumulative traffic density and a biomarker of exposure, urinary 1-hydroxypyrene-glucuronide (1-OHPG). Urinary 8-hydroxydeoxyguanosine (8-OHdG) was used as a biomarker of oxidative DNA damage. Plasma nitric oxide (NO) was measured as an indicator of oxidative stress related to traffic exhaust exposure.

Results: The mean concentration of urinary 8-OHdG was substantially higher among the exposed non-smokers (13.6 µg/g creatinine) compared with the reference non-smokers (7.3 µg/g creatinine; difference 6.3, 95% CI 3.0 to 9.6). The mean concentration of NO among the exposed (48.0 µmol/l) was also higher compared with the reference non-smokers (37.6 µmol/l; difference 10.4, 95% CI –0.4 to 21.2). In linear regression adjusting for confounding, a change in log(8-OHdG) was statistically significantly related to a unit change in log(1-OHPG) (ß = 0.372, 95% CI 0.081 to 0.663).

Conclusions: Results indicate that exposure to traffic exhausts increases oxidative DNA damage. Urinary 8-OHdG is a promising biomarker of traffic exhaust induced oxidative stress.