Assessment of DNA damage in car spray painters exposed to organic solvents by the high-throughput comet assay.

Occupational exposure as a painter is associated with DNA damage and development of cancer. Comet assay has been widely adopted as a sensitive and quantitative tool for DNA damage assessment at the individual cell level in populations exposed to genotoxics. The aim of this study was to assess the application of the high-throughput comet assay, to determine the DNA damage in car spray painters. The study population included 52 car spray painters and 52 unexposed subjects. A significant increase in the %TDNA median (p < 0.001) was observed in the exposed group in comparison to the unexposed group. Neither age (%TDNA: p = 0.913) nor time of exposure (%TDNA: p = 0.398) were significantly correlated with DNA damage. The car spray painters who consumed alcohol did not show a significant increase in DNA damage compared to nonalcohol consumers (p > 0.05). The results showed an increase in DNA breaks in car spray painters exposed to organic solvents and paints; furthermore, they demonstrated the application of high-throughput comet assay in an occupational exposure study to genotoxic agents.

Genotoxic and clastogenic effects of monohaloacetic acid drinking water disinfection by-products in primary human lymphocytes.

The haloacetic acids (HAAs) are the second-most prevalent class of drinking water disinfection by-products formed by chemical disinfectants. Previous studies have determined DNA damage and repair of HAA-induced lesions in mammalian and human cell lines; however, little is known of the genomic DNA and chromosome damage induced by these compounds in primary human cells. The aim of this study was to evaluate the genotoxic and clastogenic effects of the monoHAA disinfection by-products in primary human lymphocytes. All monoHAAs were genotoxic in primary human lymphocytes, the rank order of genotoxicity and cytotoxicity was IAA > BAA >> CAA. After 6 h of repair time, only 50% of the DNA damage (maximum decrease in DNA damage) was repaired compared to the control. This demonstrates that primary human lymphocytes are less efficient in repairing the induced damage by monoHAAs than previous studies with mammalian cell lines. In addition, the monoHAAs induced an increase in the chromosome aberration frequency as a measurement of the clastogenic effect of these compounds. These results coupled with genomic technologies in primary human cells and other mammalian non-cancerous cell lines may lead to the identification of biomarkers that may be employed in feedback loops to aid water chemists and engineers in the overall goal of producing safer drinking water.

Protective effect of galantamine against oxidative damage using human lymphocytes: a novel in vitro model.

BACKGROUND AND AIMS: Neurodegenerative disorders such as Alzheimer's disease are characterized in the initial stages by an increase in reactive oxygen species that trigger apoptosis or programmed cell death. It has been suggested that the synthetic alkaloid galantamine may offer protection against this cell loss. This investigation sought to assess the protective effect of galantamine against oxidative damage induced by hydrogen peroxide (H2O2) using human lymphocytes cultured in vitro as a model. METHODS: Cell death can be measured indirectly using cell viability testing with trypan blue. Determination of the galantamine concentrations used was made possible by the negative correlation found between galantamine concentration and average mitotic index (MI). RESULTS: Average viability of lymphocytes treated with low and medium concentrations of galantamine was significantly higher than the control. CONCLUSION: Galantamine does indeed demonstrate a protective capacity against cell damage induced by hydrogen peroxide. This finding supports the possible use of the drug in treatment of neurodegenerative diseases related to oxidative stress.