2018
DOI: 10.1016/j.freeradbiomed.2018.10.434
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Roles of intracellular and extracellular ROS formation in apoptosis induced by cold atmospheric helium plasma and X-irradiation in the presence of sulfasalazine

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Cited by 32 publications
(27 citation statements)
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“…To address this problem, a multimodality strategy was recently adopted by combining nanoparticles carrying drugs with CAP. Previously, we showed the synergism in He-CAP induced apoptosis upon exposure to hyperthermia and sulfasalazine 17 , 18 . Here, we demonstrated the size-dependent effects of 2 nm, 40 nm, and 100 nm Au-NPs.…”
Section: Discussionmentioning
confidence: 94%
“…To address this problem, a multimodality strategy was recently adopted by combining nanoparticles carrying drugs with CAP. Previously, we showed the synergism in He-CAP induced apoptosis upon exposure to hyperthermia and sulfasalazine 17 , 18 . Here, we demonstrated the size-dependent effects of 2 nm, 40 nm, and 100 nm Au-NPs.…”
Section: Discussionmentioning
confidence: 94%
“…Therefore, YGDEY has been shown to be a potent ROS scavenger that can maintain redox balance. Meanwhile, excessively generated ROS damage DNA molecules in cells and caused them abnormal function . While suffered oxidative injury from UVB, DNA was protected via pretreated YGDEY that was proven in comet assay.…”
Section: Discussionmentioning
confidence: 99%
“…CAP was shown to destroy the ultrastructure of HepG2, A549, and HeLa cells to different degrees, demonstrated in perturbed ionic fluxes, nuclear fragmentation, and organelle damage [53]. Increased intracellular ROS concentration in He-CAP treated cells was shown to reduce the intracellular pH [54]. Both intracellular ROS and pH affect Ca 2+ fluxes.…”
Section: Changed Ionic Fluxes and Ph Affect Mitochondria And Endoplasmentioning
confidence: 99%
“…Moreover, CAP treatment decreases the glutathione (GSH) levels in cells and results in the loss of mitochondrial membrane potential and cytochrome c release, leading to cell death. Pre-treating the cells with an antioxidant N-acetyl-L-cysteine (NAC) dramatically decreases the death of CAP-treated cells [54]. Disruption of mitochondrial membrane integrity in CAP treated cells [57] results in decreased ATP production and downregulation of survival PI3K/AKT/mTOR and RAS/MEK pathways [59].…”
Section: Changed Ionic Fluxes and Ph Affect Mitochondria And Endoplasmentioning
confidence: 99%