XXXX -induced DNA damage in freshly isolated brain cells compared with cultured astrocytes in the Comet assay.

@entity1 @entity64 @entity19 @entity3624 @entity26 @entity16 @entity620 @entity273 @entity2196 @entity224
Brain cells are continuously exposed to reactive @entity26 species generated by oxidative metabolism, and in certain pathological conditions defence mechanisms against @entity26 radicals may be weakened and/or overwhelmed. DNA is a potential target for oxidative damage, and genomic damage can contribute to neuropathogenesis. It is important, therefore, to identify tools for the quantitative analysis of DNA damage in models of @entity16 . The aim of this study was to compare the susceptibility of DNA to oxidative stress in cells freshly dissociated from the @entity19 brain, to that in cultured brain cells. Both primary cultures and a continuous cell line of astrocytes were considered. All cells were treated by @entity3624 / @entity3624 oxidase, a @entity224 generator or @entity273 , applied alone or in the presence of the @entity26 radical scavengers, @entity224 dismutase, @entity2196 , or ascorbic acid. DNA damage, quantified with the Comet assay, was consistent in all the different cell preparations exposed to oxidative stress, and was attenuated in similar ways by @entity224 dismutase and @entity2196 , scavengers of @entity224 anion and @entity273 , respectively. The results with @entity620 were more variable, presumably because this compound may switch from anti- to pro-oxidant status depending on its concentration and other experimental conditions. Overall, similar responses were found in freshly dissociated and cultured brain cells. These results suggest that the Comet assay can be directly applied to cells freshly dissociated from the brain of rodents, including models of @entity16 , such as @entity64 models and animals with targeted mutations that mimic @entity1 diseases.
