Regular ArticleReactive Oxygen Species Act at both TGF-β-Dependent and -Independent Steps during Induction of Apoptosis of Transformed Cells by Normal Cells
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Singlet oxygen treatment of tumor cells triggers extracellular singlet oxygen generation, catalase inactivation and reactivation of intercellular apoptosis-inducing signaling
2015, Redox BiologyCitation Excerpt :Extracellular superoxide anions generated by membrane-associated NADPH oxidase (NOX) and their dismutation product H2O2 control the proliferation of malignant cells and are involved in the maintenance of the transformed state in vitro [3–8] and in vivo [8–14]. These oncogenic effects of superoxide anions are counteracted by ROS-dependent intercellular induction of apoptosis, a process that selectively eliminates transformed cells [1,15–30]. ROS-dependent intercellular apoptosis induction is mainly based on the HOCl [1,23,24,29,30] and the NO/peroxynitrite signaling pathway [1,24,26,29,30].
Revealing mechanisms of selective, concentration-dependent potentials of 4-hydroxy-2-nonenal to induce apoptosis in cancer cells through inactivation of membrane-associated catalase
2015, Free Radical Biology and MedicineCitation Excerpt :Extracellular superoxide anion generation therefore represents a crucial step in oncogenesis and is not found in nontransformed cells [1,3,5]. The procarcinogenic effects of superoxide anions are counteracted by specific apoptosis induction in transformed cells through superoxide anion-mediated intercellular apoptosis-inducing signaling2 [17–28] (Fig. 1A), which can be established as an interplay between nontransformed and transformed cells or between the transformed cells themselves [28,29]. The efficiency as well as the selectivity of this process depends on extracellular superoxide anions of the transformed target cells.
Cytotoxic effects of incense particles in relation to oxidative stress, the cell cycle and F-actin assembly
2013, Toxicology LettersCitation Excerpt :Notably this phenomenon was observed in the cellular oxidative stress induced by time-dependent incense PM2.5 exposure, possibly resulting from the depletion of cellular antioxidant supplement with GSH (from NAC), which consequently allowed the generation of significant quantities of ROS upon exposure. A deficiency in GSH has been suggested as a signal for the induction of apoptosis (Langer et al., 1996), which aside from ROS, could pose a critical apoptotic mediator; particularly in the mitochondria which would cause irreversible apoptosis. Correlations between the inorganic compounds in incense PM2.5 and the biological responses suggest numerous inorganic elements that could play a role in regulation of oxidative stress, the cell cycle, F-actin and intracellular Ca2+ dynamics.
Nitric oxide-releasing prodrug triggers cancer cell death through deregulation of cellular redox balance
2013, Redox BiologyCitation Excerpt :We have shown previously that the rate of reaction with GSH is important for anticancer efficacy of aryl-diazeniumdiolate-based NO-releasing prodrugs [17,19]. Depletion of cellular antioxidant defenses allows for the generation of significant quantities of ROS, which have been suggested to induce apoptosis [16]. The release of NO from JS-K in the cells was confirmed by DAF fluorescence assay (Fig. 4(A)).
Effect of gold nanoparticles on glutathione depletion-induced hydrogen peroxide generation and apoptosis in HL7702 cells
2011, Toxicology LettersCitation Excerpt :Therefore, GSH has been proven to be the best defense against the potential toxicity of H2O2 in the mitochondria. Depletion of GSH allows for the generation of significant quantities of H2O2, which have been demonstrated to perform certain functions in inducing apoptosis (Langer et al., 1996), and the loss of mitochondrial membrane potential (ΔΨm) (Cook et al., 1999; Skulachev, 2006). Upon apoptotic stimulus, the cytosolic pro-apoptotic protein, such as Bax, translocates to mitochondrial membrane, which serves as a gateway for cytochrome c release (Chena and Lesnefsky, 2006; Oha and Lim, 2006) and downstream caspase 3 activation (Ghosh et al., 2005).