Detection of damage on single- or double-stranded DNA in a population exposed to arsenic in drinking water.

Different studies have suggested an association between arsenic (As) exposure and damage to single-stranded DNA by reactive oxygen species derived from the biotransformation of arsenic. The single strand damages are converted to double strand damage upon interaction with ultraviolet radiation. Analysis of genomic integrity is important for assessing the genotoxicity caused by environmental pollutants. In this study, we compared the concentration of As in drinking water, nutritional status, lifestyle variables, and the level of genotoxicity in an exposed population and a control group. Arsenic content of water was determined using a portable Arsenator® kit. DNA fragmentation was determined using the two-tailed comet assay. Our results show that the exposed population had low nutritional consumption compared to the control group (P < 0.05). Furthermore, the water consumed by the exposed group had As concentration of 14.3 ± 8.4 mg/L, whereas the As level in the water consumed by the control group was 7.7 ± 3.5 mg/L. Analysis shows that the frequency of double strand break (DSB) fragmentation was higher in the population exposed to higher levels of As compared to that of the control group. These results suggest a possible association between the concentration of As in drinking water and lifestyle variables, with increasing fragmentation of DSBs in the exposed population.

Relationship between lymphocyte DNA fragmentation and dose of iron oxide (Fe2O3) and silicon oxide (SiO2) nanoparticles.

At present, the use of nanoparticles is a controversial topic, especially when analyzing their effects in human tissues. Nanoparticles (NPs) can cause oxidative stress by increasing membrane lipids peroxidation and reactive oxygen species, and decreasing intracellular glutathione. Oxidative stress plays an important role in cell signaling and inflammatory responses. It can result in genotoxicity, affect cell proliferation, and induce DNA damage. The objective of this study is to evaluate the genotoxic potential of NPs in lymphocyte DNA. Wistar female rats (N = 45) were sorted in three randomized groups as follows: Group 1 (N = 20); Group 2 (N = 20) and a control group (N = 5). A single dose of iron oxide (Fe2O3) and silicon oxide (SiO2) NPs dissolved in saline solution were administered orally to the rats. Cardiac puncture was performed to extract peripheral blood for genotoxic analysis. DNA fragmentation for lymphocytes was performed. Control rats showed a fragmentation percentage of 11.20 ± 2.16%. Rats exposed to SiO2 and Fe2O3 NPs for 24 h showed statistically significant differences in DNA fragmentation percentages as compared with that of the control group. A lineal dose-response correlation between genotoxic damage and exposure to SiO2 and Fe2O3 NPs was found (r2 = 0.99 and 0.98 for SiO2 and Fe2O3, respectively). In conclusion, we found that exposure to Fe2O3 and SiO2 NPs can cause DNA fragmentation in lymphocytes in a dose-dependent manner.