In the past Glenda N. da Silva has collaborated on articles with Ana Paula Bazo. One of their most recent publications is Original ArticleDNA repair gene polymorphism is associated with the genetic basis of atherosclerotic coronary artery disease. Which was published in journal Cardiovascular Pathology.

More information about Glenda N. da Silva research including statistics on their citations can be found on their Copernicus Academic profile page.

Glenda N. da Silva's Articles: (2)

Original ArticleDNA repair gene polymorphism is associated with the genetic basis of atherosclerotic coronary artery disease

AbstractBackgroundAtherosclerotic coronary artery disease (CAD) is a multifactorial process that appears to be caused by the interaction of environmental risk factors with multiple predisposing genes. It is nowadays accepted that increased levels of DNA damage induced by xenobiotics play an important role in the early phases of atherogenesis. Therefore, in this study, we focus on determining whether genetic variations in xenobiotic-metabolizing [glutathione-S-transferase theta 1 (GSTT1), glutathione-S-transferase mu 1 (GSTM1), cytochrome P450 IIEI (CYP2E1)] and DNA repair [X-ray cross-complementing group 1 (XRCC1)] genes might be associated with increased risk for CAD.MethodsA case-control study was conducted with 400 individuals who underwent subjected to coronary angiography. A total of 299 were patients diagnosed with effective coronary atherosclerosis (case group; >20% obstructive lesion), and 101 (control group) were individuals diagnosed as negative for CAD (<20% obstructive lesions). The polymorphism identifications for GSTM1 and GSTT1, and for CYP2E1 and XRCC1 genes were performed by polymerase chain reaction (PCR) amplification and by PCR-RFLP, respectively.Results and conclusionsThe XRCC1 homozygous wild-type genotype Arg/Arg for codon 399 was statistically less pronounced in the case subjects (21.4%) than in controls (38.5%); individuals with the variant XRCC1 genotype had a 2.3-fold increased risk for coronary atherosclerosis than individuals with the wild-type genotype (OR=2.3, 95% CI=1.13–4.69). Conversely, no association between GSTM1, GSTT1, and CYP2E1gene polymorphisms and coronary atherosclerosis was detected. The results provide evidence of the role of DNA damage and repair in cardiovascular disease.

EndodontologyOnline only articleGenotoxicity in primary human peripheral lymphocytes after exposure to regular and white mineral trioxide aggregate

ObjectiveTaking into consideration that DNA damage plays an important role in carcinogenesis, the purpose of this study was to evaluate whether regular and white mineral trioxide aggregate (MTA) are able to induce genetic damage in primary human cells.Study designHuman peripheral lymphocytes obtained from 10 healthy volunteers were exposed to 2 presentation forms of MTA at final concentrations ranging from 1 to 1000 μg/mL for 1 hour at 37°C. The negative control group was treated with vehicle control (phosphate buffer solution, PBS) for 1 hour at 37°C and the positive control group was treated with hydrogen peroxide (at 100 μM) for 5 minutes on ice. Results were analyzed by the Friedman nonparametric test.ResultsThe results pointed out that either regular or white MTA in all concentrations tested did not induce DNA breakage in human peripheral lymphocytes as depicted by the mean tail moment.ConclusionIn summary, our results indicate that exposure to MTA may not be a factor that increases the level of DNA lesions in human peripheral lymphocytes as detected by single cell gel (comet) assay.

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