Effect of Genetic Polymorphisms of CYP2E1 and ALDH2 on the Relationship between the Levels of Urinary 8-Hydroxydeoxyguanosine and t,t-Muconic Acid

Author(s):  
Yong Dae Kim ◽  
Jong Won Kang ◽  
Sang Yong Eom ◽  
Yan Wei Zhang ◽  
Sung Hoon Kim ◽  
...  
2010 ◽  
Vol 30 (4) ◽  
pp. 338-342 ◽  
Author(s):  
Yong-Dae Kim ◽  
Sang-Yong Eom ◽  
Yan Wei Zhang ◽  
Hyeongsu Kim ◽  
Jung-Duk Park ◽  
...  

Urinary hippuric acid (HA) has been widely used as a biological marker of occupational exposure to toluene, although it is no longer valid for low levels of toluene exposure. Toluene exposure is known to induce oxidative DNA damage and the metabolism is affected by genetic polymorphisms of some metabolizing enzymes. Therefore, genetic polymorphisms of these metabolizing enzymes must be considered in the evaluation of oxidative stress caused by toluene exposure. We evaluated the relationship between urinary 8-hydroxydeoxyguanosine (8-OHdG), a marker of oxidative DNA damage, and urinary HA in individuals without occupational exposure to toluene and characterized the possible roles of GSTM1, GSTT1, and aldehyde dehydrogenase 2 (ALDH2) genotypes in the relationships between these markers. In this study, we enrolled 92 healthy Koreans. Urinary HA and 8-OHdG levels were measured and the correlations between them were statistically tested according to the GSTM1, GSTT1, and ALDH2 genotypes. HA did not significantly correlate with urinary 8-OHdG in overall subjects. However, the correlation between them showed a statistical significance in individuals with GSTM1-null, GSTT1-null, and ALDH2 *2/*2 genotypes (r = 0.766, p < 0.01). This study shows that the relationship between urinary HA and 8-OHdG concentration is modified by genetic polymorphisms of some metabolizing enzymes such as GSTM1, GSTT1, and ALDH2.


2012 ◽  
Vol 177 (11) ◽  
pp. 1359-1365 ◽  
Author(s):  
Mark E. Landau ◽  
Kimbra Kenney ◽  
Patricia Deuster ◽  
Rodney S. Gonzalez ◽  
Carmen Contreras-Sesvold ◽  
...  

2011 ◽  
Vol 38 (9) ◽  
pp. 1960-1965 ◽  
Author(s):  
DEVYANI MISRA ◽  
SARAH L. BOOTH ◽  
MICHEAL D. CROSIER ◽  
JOSE M. ORDOVAS ◽  
DAVID T. FELSON ◽  
...  

Objective.Factors associated with mineralization and osteophyte formation in osteoarthritis (OA) are incompletely understood. Genetic polymorphisms of matrix Gla protein (MGP), a mineralization inhibitor, have been associated clinically with conditions of abnormal calcification. We therefore evaluated the relationship of MGP concentrations and polymorphisms at the MGP locus to hand OA.Methods.Ours was an ancillary study to a 3-year randomized trial assessing the effect of vitamin K supplementation on vascular calcification and bone loss among community-dwelling elders. We studied participants who had serum MGP concentration measured and DNA genotyped for 3 MGP genetic polymorphisms (rs1800802, rs1800801, and rs4236), and who had hand radiographs. We evaluated the cross-sectional associations of serum MGP and the 3 MGP genetic polymorphisms, respectively, with radiographic hand OA using logistic regression with generalized estimating equations, adjusting for potential confounders.Results.Radiographic hand OA in ≥ 1 joint was present in 71% of the 376 participants (mean age 74 years, mean body mass index 28 kg/m2, 59% women). No significant association between serum MGP concentrations and radiographic hand OA was found [adjusted OR 1.0 (ref), 1.40, 1.21, and 1.21 for quartiles 1–4, respectively]. Homozygosity of the rs1800802 minor allele was associated with 0.56 times lower prevalence of hand OA compared with having ≥ 1 major allele at this locus (95% CI 0.32–0.99, p = 0.046).Conclusion.There may be an association between hand OA and genetic polymorphism at the MGP locus that is not reflected by total MGP serum concentrations. Further studies are warranted to replicate and elucidate potential mechanisms underlying these observed associations.


2017 ◽  
Vol 51 (3) ◽  
pp. 209-215 ◽  
Author(s):  
Andrea Lips ◽  
Leonardo Santos Antunes ◽  
Lívia Azeredo Antunes ◽  
Júlia Guimarães Barcellos de Abreu ◽  
Driely Barreiros ◽  
...  

The antimicrobial peptides human β-defensins (hBDs) are encoded by β-defensin genes (DEFBs) and are possibly involved in caries susceptibility. In this study we aimed (1) to investigate the relationship between salivary hBDs and caries and (2) to evaluate the association of genetic polymorphisms in DEFB1 and microRNA202 (miRNA202) with salivary levels of hBDs and caries experience. Two data sets were available for this study, totalizing 678 Brazilian children. Dental examination and saliva collection were performed in all included children. The salivary level for hDB1, hBD2, and hBD4 was assessed by ELISA sandwich technique in 168 children. The DNA was extracted from saliva, and polymorphisms in DEFB1 and miRNA202 were analyzed by real-time PCR. Statistical analysis was performed to investigate the associations between caries experience, hBD salivary level, genotype, and allele distribution, with an alpha of 0.05. The hBD1 level was significantly higher in caries-free children (p < 0.0001). The miRNA202 was associated with a lower level of salivary hBD1 (p < 0.05). Also, the polymorphic distribution of miRNA202 was associated with caries (p = 0.006). The polymorphisms in DEFB1 were not associated with hBD salivary level and caries experience (p > 0.05). In conclusion, our results indicate that genetic polymorphism in miRNA202 is involved in hBD1 salivary level as well as caries experience in children.


2020 ◽  
Vol 1 (4) ◽  
pp. 16-21
Author(s):  
Neisi Abdolkazem ◽  
Mahmoudi Parviz ◽  
Kayedi Neda ◽  
Behroozi Hamid

Benzene is known as an environmental and industrial pollutant. One way to check the amount of exposure to benzene is to measure its metabolites in the urine. Trans, Trans-Muconic Acid which is one of its metabolites is also as a biological indicator of exposure to benzene. In this study, the relationship between the amount of this biomarker and the environmental benzene concentration was investigated in two groups of policemen working outdoors in the traffic-congested areas and indoor in the same area. The results showed that the highest amount of benzene was in Salman Farsi Station at 4.44 ppm. At the same time, the biomarker measured in the urine showed 127.20 μg / L, which was the highest amount. In addition, the amount of benzene in the outdoor was approximately 3 times more than indoor and the amount of biomarker measured in outdoor employees was two times more than indoors ones. In general, wherever there was more benzene, the biomarker would also show a higher amount.


2018 ◽  
Vol 19 (3) ◽  
pp. 1-11
Author(s):  
Fadwa Elmiar ◽  
Ergin Altuner ◽  
Asuman Özgöz ◽  
Serap Demir

Epidemiology ◽  
2006 ◽  
Vol 17 (Suppl) ◽  
pp. S149-S150 ◽  
Author(s):  
M L. Kile ◽  
E A. Houseman ◽  
T J. Smith ◽  
J J. Harrington ◽  
Q Quamruzzaman ◽  
...  

2017 ◽  
Vol 33 (1) ◽  
pp. 116-123 ◽  
Author(s):  
Sílvia Soares ◽  
Augusto Nogueira ◽  
Ana Coelho ◽  
Joana Assis ◽  
Deolinda Pereira ◽  
...  

Background: Several studies have suggested that there are single nucleotide polymorphisms (SNPs) that can be considered potential biomarkers in the prognosis and therapeutic response of cancer patients. The present study investigated the association between ERCC1 rs3212986 and XRCC3 rs861539 polymorphisms and clinical toxicities induced by chemoradiotherapy (CRT) in cervical cancer. Methods: This hospital-based retrospective cohort study included 260 patients with cervical cancer, FIGO stages Ib2-IVa, who underwent CRT (cisplatin). Genetic polymorphisms analysis was performed by allelic discrimination with real-time polymerase chain reaction (RT-PCR). Results: Our results indicated a link between ERCC1 rs3212986 and the onset of late gastrointestinal toxicity (p = 0.038). Furthermore, using a recessive model (AA vs. CC/CA), we found that patients carrying AA homozygous genotype presented a fourfold increased risk of developing late gastrointestinal toxicity when compared with patients with the C allele (odds ratio = 3.727, 95% confidence interval, 1.199-11.588; p = 0.017). No association was found regarding the XRCC3 rs861539 polymorphism and any clinical toxicity event. Conclusions: This is the first study evaluating the relationship between these polymorphisms and clinical toxicities in cervical cancer patients submitted to CRT with cisplatin. These results may contribute toward a better understanding of the influence of genetic polymorphisms in genes associated with DNA repair in the clinical response to CRT of patients with cervical cancer.


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