DNA damage in multiple organs after exposure to chlorhexidine in Wistar rats.

Since chlorhexidine is effective against microorganisms, it is widely recommended in dentistry. However, studies have provided evidence that chlorhexidine is toxic for a variety of cell types. In order to identify potential genotoxins in different cell types, the purpose of this study was to investigate whether chlorhexidine digluconate is able to cause, in terms of DNA damage, alterations in leukocytes, liver, kidney and urinary bladder by the single cell gel (comet) assay. Ten male Wistar rats were divided into two groups: a negative control and the experimental group treated with 3ml of 0.12% chlorhexidine digluconate by gavage once a day for 8 days. Statistically significant increases of DNA damage was observed in leukocytes and kidney cells of the chlorhexidine digluconate treated group as depicted by the mean tail moment. Taken together, the data indicate that leukocytes and kidney cells are potential targets for primary DNA damage following oral exposure to chlorhexidine digluconate as detected by single cell gel (comet) assay.

DNA repair gene polymorphism is associated with the genetic basis of atherosclerotic coronary artery disease.

BACKGROUND: Atherosclerotic 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. METHODS: A 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 CONCLUSIONS: The 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.

Genetic damage in human peripheral lymphocytes exposed to antimicrobial endodontic agents.

OBJECTIVE: Formocresol, paramonochlorophenol, or calcium hydroxide have been widely used in dental practice to eradicate bacteria and consequently to produce root canal disinfection. Taking into consideration strong evidence for a relationship between DNA damage and carcinogenesis, the purpose of the present study was to evaluate the genotoxic effects of antimicrobial endodontic compounds in human peripheral lymphocytes by single-cell gel (comet) assay. This technique detects DNA strand breaks in individual cells. STUDY DESIGN: A total of 10 microL of the tested substance solution (formocreso1, paramonochlorofeno1, and calcium hydroxide at 100-microg/mL concentration) was added to human peripheral lymphocytes from 10 volunteers for 1 hour at 37 degrees C. The negative control group was treated with vehicle control (PBS) for 1 hour at 37 degrees C, as well. For the positive control group, lymphocytes were exposed to hydrogen peroxide at 100 microM during 5 minutes on ice. RESULTS: No DNA breakage was detected after a treatment of peripheral lymphocytes by formocresol, paramonochlorophenol, or calcium hydroxide at 100 microg/mL. CONCLUSIONS: In summary, our results indicate that exposure to formocresol, paramonochlorophenol, or calcium hydroxide may not be a factor that increases the level of DNA lesions in human peripheral lymphocytes as detected by single-cell gel (comet) assay.

Genotoxicity in primary human peripheral lymphocytes after exposure to regular and white mineral trioxide aggregate.

OBJECTIVE: Taking 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 DESIGN: Human peripheral lymphocytes obtained from 10 healthy volunteers were exposed to 2 presentation forms of MTA at final concentrations ranging from 1 to 1000 microg/mL for 1 hour at 37 degrees C. The negative control group was treated with vehicle control (phosphate buffer solution, PBS) for 1 hour at 37 degrees C and the positive control group was treated with hydrogen peroxide (at 100 microM) for 5 minutes on ice. Results were analyzed by the Friedman nonparametric test. RESULTS: The 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. CONCLUSION: In 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.