Mitochondria, oxidative stress and cell death

By M. Ott, V. Gogvadze, S. Orrenius, B. Zhivotovsky. Apoptosis, 2007

1,973 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/fe76b649a890f56cd57fcf22c69ab3e66d25fb7c

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Citations in the corpus

Oxidative stress-mediated antibacterial activity of graphene oxide and reduced graphene oxide in Pseudomonas aeruginosa (2012, background): “ROS generation is also an important factor in the apoptosis process, and the excess generation of ROS induces mitochondrial membrane permeability and damages the respiratory chain to trigger the apoptotic process.(63,64) Specific DNA smearing is a characteristic feature of cell death.”
Melatonin--a pleiotropic, orchestrating regulator molecule. (2011, background): “When interacting with cytochrome c, it gains a peroxidase activity that further promotes cardiolipin peroxidation and, ultimately, cytochrome c release (Basova et al., 2007; Bayir et al., 2007; Ott et al., 2007; Kagan et al., 2009).”
Oxidized mitochondrial DNA activates the NLRP3 inflammasome during apoptosis. (2012, background): “As both sensors and robust sources of ROS, mt rapidly respond by releasing Cyt-c and inducing apoptosis (Ott et al., 2007).”
Cytotoxicity and genotoxicity of silver nanoparticles in the human lung cancer cell line, A549 (2011, background): “Increased ROS levels have previously been implicated in the signal transduction pathways leading to apoptosis (Ott et al. 2007; Ueda et al. 2002).”
Zinc oxide nanoparticles selectively induce apoptosis in human cancer cells through reactive oxygen species (2012, background): “ROS typically include the superoxide radical (O2-), hydrogen peroxide (H 2 O 2 ), and hydroxyl radical (OH), which cause damage to cellular components including DNA and proteins.(21) In the present study, ZnO NPs significantly altered the oxidant/antioxidant status of human liver cancer cells.”
IMMUNE TOLERANCE INDUCTION BY APOPTOTIC CELLS REQUIRES CASPASE-DEPENDENT OXIDATION OF HMGB1 (2008, background): “ROS can modify cellular components and destroy their functions (Ott et al., 2007), so we reasoned that ROS might also affect apoptotic cell components involved in tolerance and immunity.”
Role of ROS and RNS Sources in Physiological and Pathological Conditions (2016, background): “Whereas the relationship between mitochondrial oxidative stress and cell death is well-established [224], that of peroxisomes in cell death pathways is just beginning to emerge.”
Ca2+ signalling checkpoints in cancer: remodelling Ca2+ for cancer cell proliferation and survival (2008, background): “As increased ROS generated by the Ca 2+ -accelerated respiratory chain promotes death, it is likely that regulation of the rate of electron transport or ROS production is crucial for avoiding cell death and tumorigenesi”
The Effects of Cadmium Toxicity (2020, background): “Excessive ROS production leads to a free radical attack of mitochondrial membrane phospholipids and mitochondrial membrane depolarization, which is a key step in the intrinsic pathway of apoptosis [85,86].”
Ferroptosis in cancer: from molecular mechanisms to therapeutic strategies (2024, background): “This 277 – 280 Therefore, further research is required to clarify the permissive or regulatory role of autophagy in the process of ferroptosis.”