@entity1063 Reduces Reactive XXXX Species (ROS) and DNA Damage in Ovarian Surface Epithelial Cells.

@entity26 @entity7361 @entity273 @entity1732 @entity1063
OBJECTIVE: To determine the role of @entity1063 (NE) on DNA damage and reactive @entity26 species (ROS) generation in ovarian surface epithelial cells. METHOD: Non-tumorigenic, immortalized ovarian surface epithelial cells were treated with NE, @entity1732 , and @entity1732 followed by NE. The comet assay was performed on each treatment group to determine the amount of single and double-strand breaks induced by treatments. ROS levels for each treatment group were measured using the @entity7361 fluorescence assay. Finally, RNA transcripts were measured for each treatment group with regards to the expression of DNA repair and oxidative stress genes. RESULTS: The mean tail moment of untreated cells was significantly greater than that of cells treated with NE (p=0.02). The mean tail moment of cells treated with @entity1732 was significantly greater than that of cells treated with @entity1732 followed by NE (p<0.01). Treatment with NE resulted in significantly less ROS generation than in untreated cells (p<0.01). NE treatment after @entity273 treatment resulted in a noticeable decrease in ROS generation. Genes associated with oxidative stress were upregulated in cells treated with @entity1732 , however this upregulation was blunted when @entity1732 -treated cells were treated subsequently with NE. CONCLUSION: NE is associated with decreased DNA damage and ROS production in ovarian surface epithelial cells. This effect is protective in the presence of the oxidative-damaging agent @entity1732 . These results suggest an additional physiologic role for the stress hormone NE, in protecting ovarian surface epithelial cells from oxidative stress.
