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OBJECTIVE: To explore the effect of occupational lead exposure on the relative telomere length(RTL) and mRNA expression of telomere-binding protein POT1-interacting protein 1(TPP1) in peripheral blood of workers. METHODS: A total of 303 workers exposed to lead were selected as the exposure group and 72 administrative logisticians personnel in the same factory as the control group using the simple random sampling method. Their peripheral blood samples were collected and were used to detect the blood lead level by Graphite furnace atomic absorption spectrometry. RTL and the relative expression of TPP1 mRNA by real-time quantitative polymerase chain reaction. RESULTS: The blood lead level of the exposure group was higher [Media(M): 68.2 vs 266.1 μg/L, P<0.01], the RTL was shorter(M: 0.96 vs 0.70, P<0.01), and the relative mRNA expression of TPP1 was lower(M: 0.92 vs 0.51, P<0.01) compared with the control group. Spearman correlation analysis results showed that the blood lead level were both negatively correlated with RTL [Spearman correlation coefficient(r_S) =-0.18, P<0.01], and the relative mRNA expression of TPP1(r_S=-0.19, P<0.01), while the RTL was positively correlated with the risk of RTL shortening and the relative mRNA expression of TPP1 decline was increased in lead exposure(P<0.01). CONCLUSION: Lead exposure can shorten the RTL and reduce the relative mRNA expression of TPP1 in workers. The mechanism may be that lead interferes with telomere repair process by inhibiting the mRNA expression of TPP1.
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OBJECTIVE: To analyze chromosome damage and its possible influencing factors in patients with occupational chronic benzene poisoning. METHODS: Fifty patients with occupational chronic benzene poisoning were selected as chronic benzene poisoning group,and 53 workers without occupational exposure to benzene and other toxic substances were chosen as control group by using convenience sampling method. Questionnaire and routine blood test were conducted on all study subjects. Micronucleus rate test was performed by micronucleus blocking cytokinesis assay. RESULTS: Peripheral blood tests of chronic benzene poisoning group showed significantly reduced hemoglobin level,counts of red blood cells,white blood cells,platelets,lymphocytes and neutrophils( P < 0. 01),and higher lymphocyte micronucleus rates compared to control group( !: 6. 26‰ vs 3. 91‰,P < 0. 01). The proportion of increased lymphocyte micronucleus rate in chromic benzene poisoning group was also higher than that in control group( 46. 0% vs 5. 7%,P < 0. 01). The multivariate Poisson analysis results indicated that the time after disengagement from benzene exposure was the influencing factor of micronucleus rate in chronic benzene poisoning group( P < 0. 05),after adjusting the confounding factors of gender,age,smoking status,alcohol drinking status and working age of benzene exposure. CONCLUSION: Occupational chronic benzene poisoning leads to increase of chromosome damage in lymphocytes of patients. The time after disengagement from benzene exposure was positively correlated with chromosome damage.
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<p><b>OBJECTIVE</b>To evaluate the effects of polymorphisms in XRCC1 and APE1 genes on vinyl chloride (VC)-induced chromosomal damage in peripheral lymphocytes.</p><p><b>METHODS</b>In this study, 317 workers occupationally exposed to VC were recruited from a factory in Shandong Province, China. The micronucleus (MN) frequency in peripheral lymphocytes was used as an indicator of chromosomal damage. Polymerase chain reaction-restriction fragment length polymorphism and created restriction site combined with restriction fragment length polymorphism were used to determine the five single nucleotide polymorphisms in XRCC1 and APE1 genes in the base excision repair pathway. The association of chromosomal damage with these polymorphisms and the haplotype of XRCC1 was analyzed using Poisson regression and PHASE 2.0.2.</p><p><b>RESULTS</b>It was found that among the VC-exposed workers, individuals with XRCC1 polymorphisms (-77C/T, Arg194Trp, Arg280His, and Arg399Gln) had a significantly higher MN frequency than those with homozygous wild-type genotypes, with frequency ratios (FR) as follows, respectively: FR = 1.21, 95%CI: 1.05∼1.39 (P < 0.05); FR = 1.14, 95%CI: 1.00∼1.38 (P < 0.05); FR = 1.26, 95%CI: 1.11∼1.44 (P < 0.05); FR = 1.23, 95%CI: 1.08∼1.46 (P < 0.05). APE1 Asp148Glu was found of no significant relationship with MN frequency. Haplotype analysis of XRCC1 demonstrated that the MN frequencies in subjects with CTAA/CTAA and CCAA/CTAA were significantly higher than that in those with TCGG/TCGG (FR = 1.19, 95%CI: 1.02∼1.32, P < 0.05; FR = 1.41, 95%CI: 1.02∼1.87, P < 0.05). Furthermore, association was found between accumulated exposure to VC and XRCC1 polymorphisms (-77C/T, Arg194Trp, Arg280His, and Arg399Gln) after adjustment for age, sex, drinking, and smoking.</p><p><b>CONCLUSION</b>VC can induce chromosomal damage even when the exposure level is lower than the national occupational health standard of China (PC-TWA: 10 mg/m(3)); the polymorphisms in XRCC1 and APE1 are associated with chromosomal damage induced by VC.</p>
Subject(s)
Adult , Female , Humans , Male , Middle Aged , Young Adult , DNA-(Apurinic or Apyrimidinic Site) Lyase , Genetics , DNA-Binding Proteins , Genetics , Haplotypes , Micronuclei, Chromosome-Defective , Occupational Exposure , Polymorphism, Restriction Fragment Length , Vinyl Chloride , Poisoning , X-ray Repair Cross Complementing Protein 1ABSTRACT
<p><b>OBJECTIVE</b>To explore the relation between genetic polymorphisms of NQO1, GSTT1 and risks of chronic benzene poisoning (BP).</p><p><b>METHODS</b>A case-control study was conducted. 152 BP patients and 152 workers occupationally exposed to benzene without poisoning manifestations were investigated. Polymerase chain reaction (PCR), denaturing high-performance liquid chromatography(DHPLC) and sequencing were used to detect the single nucleotide polymorphisms(SNPs) of the promoter and complete coding-region of NQO1 gene. Multiple PCR was used to detect GSTT1 genotype.</p><p><b>RESULTS</b>In smoking population, there was 7.73-fold (95% CI: 1.71-34.97, P = 0.010) of risk in BP subjects carrying NQO1c. 609 T/T genotype, compared with those carrying C/C and C/T. genotype. In drinking population, the individuals carrying the 6th extron of NQO1c. 609 T/T homozygote genotype had a 11.00-fold(95% CI: 1.89-63.83, P = 0.005) risk of BP compared to those with NQO1c. 609 C/T and C/C genotypes.</p><p><b>CONCLUSION</b>The subjects carrying NQO1c. 609 T/T genotype and together with the habit of smoking or drinking may be more susceptible to BP.</p>