ROS induced DNA damage and checkpoint responses: Influences on aging?

Tp53-induced Glycolysis and Apoptosis Regulator (TIGAR) Protects Glioma Cells from Starvation-induced Cell Death by Up-regulating Respiration and Improving Cellular Redox Homeostasis

“…Oxidative phosphorylation is by far more efficient in ATP generation per mol of glucose, but it also leads to raised intracellular ROS 2 levels (3,4). Although ROS can play important roles in regulating cell signaling and homeostasis when present in moderate quantity (5)(6)(7)(8)(9)(10)(11), excessive amounts can damage cellular components such as proteins or DNA (12)(13)(14)(15). ROS homeostasis is dependent on NADPH generation through the pentose phosphate pathway (PPP) and subsequent production of reduced glutathione.…”

Oxidative Stress Facilitates IFN-γ-Induced Mimic Extracellular Trap Cell Death in A549 Lung Epithelial Cancer Cells

“…Because oxidative stress is involved in DNA damage [23], we hypothesize that IFN-γ-induced ROS generation is important for triggering the DNA damage that precedes mimic ETosis induction. As demonstrated through immunostaining, IFN-γ-induced phospho-γ-H2AX positivity was significantly ( P < 0.001) lower in A549 cells with p47 phox silencing (Fig 5A).…”

“…In IFN-γ-induced mimic ETosis, we suggest that autophagy and ROS are concomitantly involved. Oxidative stress causes DNA damage by triggering checkpoint activation in the cell cycle [23]. We previously showed that ATR/ATM mediates mimic ETosis after DNA damage by regulating PAD4-mediated citrullination of histone H3 [11].…”

Telomere loss in Philadelphia-negative hematopoiesis after successful treatment of chronic myeloid leukemia: Evidence for premature aging of the myeloid compartment

“…This is mostly due to mechanisms such as senescence that limit proliferation and survival of cells undergoing excessive telomere erosion. In normal tissues, telomeres are effective sensors of genetic damage induced by multiple stressors; most notably proliferation and oxidative damage (Passos et al, 2007;Guachalla and Rudolph, 2010).The consequences of severe telomere shortening in non-neoplastic hematopoietic cells have yet to be fully elucidated. Several reports have shown that extensive telomere shortening occurs in aplastic anemia and following severe iatrogenic stress such as chemotherapy or transplantation (Calado and Young, 2008;Ricca et al, 2005;Fig.…”

“…A physiological consequence of telomere function is the progressive shortening of telomeres in the vast majority of somatic tissues during normal life (Aubert and Lansdorp, 2008;Brü mmendorf and Balabanov, 2006). Several reports indicate that non-physiological stresses such as extensive proliferation or oxidative stress induce accelerated telomere shortening in both extra-hematopoietic and hematopoietic tissues (Brü mmendorf and Balabanov, 2006;Passos et al, 2007;Guachalla and Rudolph, 2010). Moreover also the genetic background plays a major role in telomere dynamics as the presence of hypomorphic mutations of h-TERT and other genes have shown to be associated to accelerated telomere shortening Xin et al, 2007).…”