Role of intracellular labile iron, ferritin, and antioxidant defence in resistance of chronically adapted Jurkat T cells to hydrogen peroxide

@inproceedings{AlQenaei2014RoleOI,
  title={Role of intracellular labile iron, ferritin, and antioxidant defence in resistance of chronically adapted Jurkat T cells to hydrogen peroxide},
  author={Abdullah Al-Qenaei and Anthie Yiakouvaki and Olivier Reelfs and Paolo Santambrogio and Sonia Levi and Nick D. Hall and Rex Michael Tyrrell and Charareh Pourzand},
  booktitle={Free radical biology & medicine},
  year={2014}
}
To examine the role of intracellular labile iron pool (LIP), ferritin (Ft), and antioxidant defence in cellular resistance to oxidative stress on chronic adaptation, a new H2O2-resistant Jurkat T cell line "HJ16" was developed by gradual adaptation of parental "J16" cells to high concentrations of H2O2. Compared to J16 cells, HJ16 cells exhibited much higher resistance to H2O2-induced oxidative damage and necrotic cell death (up to 3mM) and had enhanced antioxidant defence in the form of… CONTINUE READING

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Compared to J16 cells , HJ16 cells exhibited much higher resistance to H2O2-induced oxidative damage and necrotic cell death ( up to 3mM ) and had enhanced antioxidant defence in the form of significantly higher intracellular glutathione and mitochondrial ferritin ( FtMt ) levels as well as higher glutathione - peroxidase ( GPx ) activity .
Compared to J16 cells , HJ16 cells exhibited much higher resistance to H2O2-induced oxidative damage and necrotic cell death ( up to 3mM ) and had enhanced antioxidant defence in the form of significantly higher intracellular glutathione and mitochondrial ferritin ( FtMt ) levels as well as higher glutathione - peroxidase ( GPx ) activity .
Compared to J16 cells , HJ16 cells exhibited much higher resistance to H2O2-induced oxidative damage and necrotic cell death ( up to 3mM ) and had enhanced antioxidant defence in the form of significantly higher intracellular glutathione and mitochondrial ferritin ( FtMt ) levels as well as higher glutathione - peroxidase ( GPx ) activity .
Compared to J16 cells , HJ16 cells exhibited much higher resistance to H2O2-induced oxidative damage and necrotic cell death ( up to 3mM ) and had enhanced antioxidant defence in the form of significantly higher intracellular glutathione and mitochondrial ferritin ( FtMt ) levels as well as higher glutathione - peroxidase ( GPx ) activity .
Compared to J16 cells , HJ16 cells exhibited much higher resistance to H2O2-induced oxidative damage and necrotic cell death ( up to 3mM ) and had enhanced antioxidant defence in the form of significantly higher intracellular glutathione and mitochondrial ferritin ( FtMt ) levels as well as higher glutathione - peroxidase ( GPx ) activity .
Compared to J16 cells , HJ16 cells exhibited much higher resistance to H2O2-induced oxidative damage and necrotic cell death ( up to 3mM ) and had enhanced antioxidant defence in the form of significantly higher intracellular glutathione and mitochondrial ferritin ( FtMt ) levels as well as higher glutathione - peroxidase ( GPx ) activity .
Compared to J16 cells , HJ16 cells exhibited much higher resistance to H2O2-induced oxidative damage and necrotic cell death ( up to 3mM ) and had enhanced antioxidant defence in the form of significantly higher intracellular glutathione and mitochondrial ferritin ( FtMt ) levels as well as higher glutathione - peroxidase ( GPx ) activity .
Compared to J16 cells , HJ16 cells exhibited much higher resistance to H2O2-induced oxidative damage and necrotic cell death ( up to 3mM ) and had enhanced antioxidant defence in the form of significantly higher intracellular glutathione and mitochondrial ferritin ( FtMt ) levels as well as higher glutathione - peroxidase ( GPx ) activity .
Compared to J16 cells , HJ16 cells exhibited much higher resistance to H2O2-induced oxidative damage and necrotic cell death ( up to 3mM ) and had enhanced antioxidant defence in the form of significantly higher intracellular glutathione and mitochondrial ferritin ( FtMt ) levels as well as higher glutathione - peroxidase ( GPx ) activity .
Further adaptive responses include the significantly reduced cellular response to oxidant - mediated glutathione depletion , FtH modulation , and labile iron release and a significant increase in FtMt levels following H2O2 treatment .
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