PURPOSE: To determine whether changes in oxidative stress could enhance the sensitivity of neural precursor cells to ionizing radiation. MATERIALS AND METHODS: Two strategies were used whereby oxidative stress was modulated endogenously, through manipulation cell culture density, or exogenously, through direct addition of hydrogen peroxide. RESULTS: Cells subjected to increased endogenous oxidative stress through low-density growth routinely exhibited an inhibition of growth following irradiation. However, cells subjected to chronic exogenous oxidative treatments showed increased sensitivity to proton and gamma-irradiation compared to untreated controls. Reduced survival of irradiated cultures subjected to oxidizing conditions was corroborated using enzymatic viability assays, and was observed over a range of doses (1 - 5 Gy) and post-irradiation re-seeding densities (20 - 200 K/plate). CONCLUSIONS: Collectively our results provide further support for the importance of redox state in the regulation of neural precursor cell function, and suggest that oxidative stress can inhibit the proliferative potential of cells through different mechanisms. This is likely to compromise survival and under conditions where excess exogenous oxidants might predominate, sensitivity to irradiation may be enhanced.
PURPOSE: To determine whether changes in oxidative stress could enhance the sensitivity of neural precursor cells to ionizing radiation. MATERIALS AND METHODS: Two strategies were used whereby oxidative stress was modulated endogenously, through manipulation cell culture density, or exogenously, through direct addition of hydrogen peroxide. RESULTS: Cells subjected to increased endogenous oxidative stress through low-density growth routinely exhibited an inhibition of growth following irradiation. However, cells subjected to chronic exogenous oxidative treatments showed increased sensitivity to proton and gamma-irradiation compared to untreated controls. Reduced survival of irradiated cultures subjected to oxidizing conditions was corroborated using enzymatic viability assays, and was observed over a range of doses (1 - 5 Gy) and post-irradiation re-seeding densities (20 - 200 K/plate). CONCLUSIONS: Collectively our results provide further support for the importance of redox state in the regulation of neural precursor cell function, and suggest that oxidative stress can inhibit the proliferative potential of cells through different mechanisms. This is likely to compromise survival and under conditions where excess exogenous oxidants might predominate, sensitivity to irradiation may be enhanced.
Authors: N Y Calingasan; D J Ho; E J Wille; M V Campagna; J Ruan; M Dumont; L Yang; Q Shi; G E Gibson; M F Beal Journal: Neuroscience Date: 2008-03-18 Impact factor: 3.590
Authors: Son T Ton; Shih-Yen Tsai; Ian C Vaagenes; Kelly Glavin; Joanna Wu; Jonathan Hsu; Hannah M Flink; Daniel Nockels; Timothy E O'Brien; Gwendolyn L Kartje Journal: J Neurosci Res Date: 2019-01-07 Impact factor: 4.164
Authors: Tatiana B Krasieva; Erich Giedzinski; Katherine Tran; Mary Lan; Charles L Limoli; Bruce J Tromberg Journal: J Innov Opt Health Sci Date: 2011-07-01
Authors: Bertrand P Tseng; Mary L Lan; Katherine K Tran; Munjal M Acharya; Erich Giedzinski; Charles L Limoli Journal: Redox Biol Date: 2013-01-19 Impact factor: 11.799