Abstract
Aims
HCT116 cells were treated with H2O2 concentrations from 1–10 mM to induce oxidative stress and the effect on cell viability was examined using the XTT assay. Under the conditions tested, even at the highest concentration only a minimal decrease in viability was observed (~10%), so for subsequent experiments cells were treated with 1–5 mM H2O2 for 30 mins. Activation of the Akt signaling pathway (measured by phospho-Akt) and interaction with the key redox proteins thioredoxin (Trx) and
Results
Changes were seen in the levels of Trx and Prdx dimers, which appeared to decrease following oxidative stress. Interestingly, while moderate levels of H2O2 (1 mM) induced activation of the Akt pathway, treatment with higher concentrations caused a decrease in p-Akt levels. This suggests that oxidation of PTEN during moderate oxidative stress inhibits the PI3K/Akt pathway, but under more severe conditions this effect is reversed. Further work is required to identify the mechanisms of this effect.
HCT116 cells were treated with H2O2 concentrations from 1–10 mM to induce oxidative stress and the effect on cell viability was examined using the XTT assay. Under the conditions tested, even at the highest concentration only a minimal decrease in viability was observed (~10%), so for subsequent experiments cells were treated with 1–5 mM H2O2 for 30 mins. Activation of the Akt signaling pathway (measured by phospho-Akt) and interaction with the key redox proteins thioredoxin (Trx) and
Results
Changes were seen in the levels of Trx and Prdx dimers, which appeared to decrease following oxidative stress. Interestingly, while moderate levels of H2O2 (1 mM) induced activation of the Akt pathway, treatment with higher concentrations caused a decrease in p-Akt levels. This suggests that oxidation of PTEN during moderate oxidative stress inhibits the PI3K/Akt pathway, but under more severe conditions this effect is reversed. Further work is required to identify the mechanisms of this effect.
Original language | English |
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Pages (from-to) | S57-S58 |
Number of pages | 3 |
Journal | Free Radical Biology and Medicine |
Volume | 96 |
Issue number | Supplement 1 |
DOIs | |
Publication status | Published - 1 Jul 2016 |