Reactive oxygen species involvement in apoptosis and mitochondrial damage in Caco-2 cells induced by enniatins A, A1, B and B1

2013 ◽  
Vol 222 (1) ◽  
pp. 36-44 ◽  
Author(s):  
A. Prosperini ◽  
A. Juan-García ◽  
G. Font ◽  
M.J. Ruiz
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Mitochondrial Damage ◽  
Oxygen Species

scholarly journals Mechanisms of Mitochondrial Damage in Keratinocytes by Pemphigus Vulgaris Antibodies

2013 ◽  
Vol 288 (23) ◽  
pp. 16916-16925 ◽  
Author(s):  
Mina Kalantari-Dehaghi ◽  
Yumay Chen ◽  
Wu Deng ◽  
Alex Chernyavsky ◽  
Steve Marchenko ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Mouse Skin ◽  
Reactive Oxygen ◽  
Pemphigus Vulgaris ◽  
Mitochondrial Damage ◽  
Response To Treatment ◽  
Transfer Model ◽  
Clear Understanding ◽  
Oxygen Species ◽  
Mitochondrial Functions

The development of nonhormonal treatment of pemphigus vulgaris (PV) has been hampered by a lack of clear understanding of the mechanisms leading to keratinocyte (KC) detachment and death in pemphigus. In this study, we sought to identify changes in the vital mitochondrial functions in KCs treated with the sera from PV patients and healthy donors. PV sera significantly increased proton leakage from KCs, suggesting that PV IgGs increase production of reactive oxygen species. Indeed, measurement of intracellular reactive oxygen species production showed a drastic increase of cell staining in response to treatment by PV sera, which was confirmed by FACS analysis. Exposure of KCs to PV sera also caused dramatic changes in the mitochondrial membrane potential detected with the JC-1 dye. These changes can trigger the mitochondria-mediated intrinsic apoptosis. Although sera from different PV patients elicited unique patterns of mitochondrial damage, the mitochondria-protecting drugs nicotinamide (also called niacinamide), minocycline, and cyclosporine A exhibited a uniform protective effect. Their therapeutic activity was validated in the passive transfer model of PV in neonatal BALB/c mice. The highest efficacy of mitochondrial protection of the combination of these drugs found in mitochondrial assay was consistent with the ability of the same drug combination to abolish acantholysis in mouse skin. These findings provide a theoretical background for clinical reports of the efficacy of mitochondria-protecting drugs in PV patients. Pharmacological protection of mitochondria and/or compensation of an altered mitochondrial function may therefore become a novel approach to development of personalized nonhormonal therapies of patients with this potentially lethal autoimmune blistering disease.

IFN-β-induced reactive oxygen species and mitochondrial damage contribute to muscle impairment and inflammation maintenance in dermatomyositis

2017 ◽  
Vol 134 (4) ◽  
pp. 655-666 ◽  
Author(s):  
Alain Meyer ◽  
Gilles Laverny ◽  
Yves Allenbach ◽  
Elise Grelet ◽  
Vanessa Ueberschlag ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Mitochondrial Damage ◽  
Oxygen Species ◽  
Muscle Impairment

Albumin prevents reactive oxygen species-induced mitochondrial damage, autophagy, and apoptosis during serum starvation

APOPTOSIS ◽  
2012 ◽  
Vol 17 (11) ◽  
pp. 1156-1169 ◽  
Author(s):  
Shu-Yu Liu ◽  
Chia-Ling Chen ◽  
Tsan-Tzu Yang ◽  
Wei-Ching Huang ◽  
Chia-Yuan Hsieh ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Mitochondrial Damage ◽  
Serum Starvation ◽  
Oxygen Species

scholarly journals Methylglyoxal-Induced Dysfunction in Brain Endothelial Cells via the Suppression of Akt/HIF-1α Pathway and Activation of Mitophagy Associated with Increased Reactive Oxygen Species

Antioxidants ◽  
2020 ◽  
Vol 9 (9) ◽  
pp. 820 ◽  
Author(s):  
Donghyun Kim ◽  
Kyeong-A Kim ◽  
Jeong-Hyeon Kim ◽  
Eun-Hye Kim ◽  
Ok-Nam Bae
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Endothelial Cells ◽  
Tight Junction ◽  
Reactive Oxygen ◽  
Mitochondrial Damage ◽  
Oxygen Species ◽  
Brain Endothelial Cells ◽  
Tight Junction Proteins ◽  
Junction Proteins

Methylglyoxal (MG) is a dicarbonyl compound, the level of which is increased in the blood of diabetes patients. MG is reported to be involved in the development of cerebrovascular complications in diabetes, but the exact mechanisms need to be elucidated. Here, we investigated the possible roles of oxidative stress and mitophagy in MG-induced functional damage in brain endothelial cells (ECs). Treatment of MG significantly altered metabolic stress as observed by the oxygen-consumption rate and barrier-integrity as found in impaired trans-endothelial electrical resistance in brain ECs. The accumulation of MG adducts and the disturbance of the glyoxalase system, which are major detoxification enzymes of MG, occurred concurrently. Reactive oxygen species (ROS)-triggered oxidative damage was observed with increased mitochondrial ROS production and the suppressed Akt/hypoxia-inducible factor 1 alpha (HIF-1α) pathway. Along with the disturbance of mitochondrial bioenergetic function, parkin-1-mediated mitophagy was increased by MG. Treatment of N-acetyl cysteine significantly reversed mitochondrial damage and mitophagy. Notably, MG induced dysregulation of tight junction proteins including occludin, claudin-5, and zonula occluden-1 in brain ECs. Here, we propose that diabetic metabolite MG-associated oxidative stress may contribute to mitochondrial damage and autophagy in brain ECs, resulting in the dysregulation of tight junction proteins and the impairment of permeability.

Reactive oxygen species, heat stress and oxidative-induced mitochondrial damage. A review

2014 ◽  
Vol 30 (7) ◽  
pp. 513-523 ◽  
Author(s):  
Imen Belhadj Slimen ◽  
Taha Najar ◽  
Abdeljelil Ghram ◽  
Hajer Dabbebi ◽  
Moncef Ben Mrad ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Heat Stress ◽  
Reactive Oxygen ◽  
Mitochondrial Damage ◽  
Oxygen Species

Diazoxide prevents reactive oxygen species and mitochondrial damage, leading to anti-hypertrophic effects

2017 ◽  
Vol 261 ◽  
pp. 50-55 ◽  
Author(s):  
Aline M. Lucas ◽  
Francisco R. Caldas ◽  
Amanda P. da Silva ◽  
Maximiano M. Ventura ◽  
Iago M. Leite ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Mitochondrial Damage ◽  
Oxygen Species

scholarly journals Hepatitis C Virus Triggers Mitochondrial Permeability Transition with Production of Reactive Oxygen Species, Leading to DNA Damage and STAT3 Activation

2006 ◽  
Vol 80 (14) ◽  
pp. 7199-7207 ◽  
Author(s):  
Keigo Machida ◽  
Kevin T.-H. Cheng ◽  
Chao-Kuen Lai ◽  
King-Song Jeng ◽  
Vicky M.-H. Sung ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Dna Damage ◽  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Reactive Oxygen ◽  
Mitochondrial Damage ◽  
Hcv Infection ◽  
Oxygen Species ◽  
Dna Breaks ◽  
Infected Cells

ABSTRACT Hepatitis C virus (HCV) infection is frequently associated with the development of hepatocellular carcinomas and non-Hodgkin's B-cell lymphomas. Previously, we reported that HCV infection causes cellular DNA damage and mutations, which are mediated by nitric oxide (NO). NO often damages mitochondria, leading to induction of double-stranded DNA breaks (DSBs) and accumulation of oxidative DNA damage. Here we report that HCV infection causes production of reactive oxygen species (ROS) and lowering of mitochondrial transmembrane potential (ΔΨm) in in vitro HCV-infected cell cultures. The changes in membrane potential could be inhibited by BCL-2. Furthermore, an inhibitor of ROS production, antioxidant N-acetyl-l-cysteine (NAC), or an inhibitor of NO, 1400W, prevented the alterations of ΔΨm. The HCV-induced DSB was also abolished by a combination of NO and ROS inhibitors. These results indicated that the mitochondrial damage and DSBs in HCV-infected cells were mediated by both NO and ROS. Among the HCV proteins, core, E1, and NS3 are potent ROS inducers: their expression led to DNA damage and activation of STAT3. Correspondingly, core-protein-transgenic mice showed elevated levels of lipid peroxidation and oxidatively damaged DNA. These HCV studies thus identified ROS, along with the previously identified NO, as the primary inducers of DSBs and mitochondrial damage in HCV-infected cells.

scholarly journals Biodegradable hollow mesoporous organosilica nanotheranostics  (HMON) for multi-mode imaging and mild photo-therapeutic-induced mitochondrial damage on gastric cancer

2020 ◽  
Author(s):  
Weihong Guo ◽  
Zhian Chen ◽  
Jiajia Chen ◽  
Xiaoli Feng ◽  
Yang Yang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Reactive Oxygen Species ◽  
Cell Apoptosis ◽  
Reactive Oxygen ◽  
Mitochondrial Damage ◽  
Oxygen Species ◽  
Apoptosis Pathway ◽  
Mesoporous Organosilica ◽  
Apoptotic Protein

Abstract Background: CuS-modified hollow mesoporous organosilica nanoparticles (HMON@CuS) have been preferred as non-invasive treatment for cancer, as near infrared (NIR)-induced photo-thermal effect (PTT) and/or photo-dynamic effect (PDT) could increase cancer cells’ apoptosis. However, the certain role of HMON@CuS-produced-PTT&PDT inducing gastric cancer (GC) cells’ mitochondrial damage, remained unclear. Moreover, theranostic efficiency of HMON@CuS might be well improved by applying multi-modal imaging, which could offer an optimal therapeutic region and time window. Herein, new nanotheranostics agents were reported by Gd doped HMON decorated by CuS nanocrystals (called HMON@CuS/Gd).Results: HMON@CuS/Gd exhibited appropriate size distribution, good biocompatibility, L-Glutathione (GSH) responsive degradable properties, high photo-thermal conversion efficiency (82.4%) and a simultaneous reactive oxygen species (ROS) generation effect. Meanwhile, HMON@CuS/Gd could efficiently enter GC cells, induce combined mild PTT (43-45 °C) and PDT under mild NIR power density (0.8W/cm2). Surprisingly, it was found that PTT might not be the only factor of cell apoptosis, as ROS induced by PDT also seemed playing an essential role. The NIR-induced ROS could attack mitochondrial transmembrane potentials (MTPs), then promote mitochondrial reactive oxygen species (mitoROS) production. Meanwhile, mitochondrial damage dramatically changed the expression of anti-apoptotic protein (Bcl-2) and pro-apoptotic protein (Bax). Since that, mitochondrial permeability transition pore (mPTP) was opened, followed by inducing more cytochrome c (Cyto C) releasing from mitochondria into cytosol, and finally activated caspase-9/caspase-3-depended cell apoptosis pathway. Our in vivo data also showed that HMON@CuS/Gd exhibited good fluorescence (FL) imaging (wrapping fluorescent agent), enhanced T1 imaging under magnetic resonance imaging (MRI) and infrared thermal (IRT) imaging capacities. Guided by FL/MRI/ IRT trimodal imaging, HMON@CuS/Gd could selectively cause mild photo-therapy at cancer region, efficiently inhibit the growth of GC cells without evident systemic toxicity in vivo. Conclusion: HMON@CuS/Gd could serve as a promising multifunctional nanotheranostic platform and as a cancer photo-therapy agent through inducing mitochondrial dysfunction on GC.

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