Permeability of inner mitochondrial membrane and oxidative stress

1988 ◽  
Vol 943 (2) ◽  
pp. 245-255 ◽  
Author(s):  
Donatella Carbonera ◽  
Giovanni Felice Azzone
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Membrane ◽  
Inner Mitochondrial Membrane ◽  
And Oxidative Stress

scholarly journals Sodium para-aminosalicylic acid inhibits manganese-induced NLRP3 inflammasome-dependent pyroptosis by inhibiting NF-κB pathway activation and oxidative stress

2020 ◽  
Vol 17 (1) ◽  
Author(s):  
Dongjie Peng ◽  
Junyan Li ◽  
Yue Deng ◽  
Xiaojuan Zhu ◽  
Lin Zhao ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Membrane Potential ◽  
Basal Ganglia ◽  
Mitochondrial Membrane Potential ◽  
Nlrp3 Inflammasome ◽  
Mitochondrial Membrane ◽  
Aminosalicylic Acid ◽  
Pathway Activation ◽  
Bv2 Cells ◽  
And Oxidative Stress

Abstract Background The activation of NOD-like receptor protein 3 (NLRP3) inflammasome-dependent pyroptosis has been shown to play a vital role in the pathology of manganese (Mn)-induced neurotoxicity. Sodium para-aminosalicylic acid (PAS-Na) has a positive effect on the treatment of manganism. However, the mechanism is still unclear. We hypothesized that PAS-Na might act through NLRP3. Methods The microglial cell line BV2 and male Sprague-Dawley rats were used to investigate the impacts of PAS-Na on Mn-induced NLRP3 inflammasome-dependent pyroptosis. The related protein of the NF-κB pathway and NLRP3-inflammasome-dependent pyroptosis was detected by western blot. The reactive oxygen species and mitochondrial membrane potential were detected by immunofluorescence staining and flow cytometry. The activation of microglia and the gasdermin D (GSDMD) were detected by immunofluorescence staining. Results Our results showed that Mn treatment induced oxidative stress and activated the NF-κB pathway by increasing the phosphorylation of p65 and IkB-α in BV2 cells and in the basal ganglia of rats. PAS-Na could alleviate Mn-induced oxidative stress damage by inhibiting ROS generation, increasing mitochondrial membrane potential and ATP levels, thereby reducing the phosphorylation of p65 and IkB-α. Besides, Mn treatment could activate the NLRP3 pathway and promote the secretion of IL-18 and IL-1β, mediating pyroptosis in BV2 cells and in the basal ganglia and hippocampus of rats. But an inhibitor of NF-κb (JSH-23) treatment could significantly reduce LDH release, the expression of NLRP3 and Cleaved CASP1 protein and IL-1β and IL-18 mRNA level in BV2 cells. Interestingly, the effect of PAS-Na treatment in Mn-treated BV2 cells is similar to those of JSH-23. Besides, immunofluorescence results showed that PAS-Na reduced the increase number of activated microglia, which stained positively for GSDMD. Conclusion PAS-Na antagonized Mn-induced NLRP3 inflammasome dependent pyroptosis through inhibiting NF-κB pathway activation and oxidative stress.

Biomedical Imaging and Visualization Model of Mitochondrial Dysfunction and Oxidative Stress in Alzheimer Disease

2011 ◽  
Vol 138-139 ◽  
pp. 1179-1182
Author(s):  
Chang Jun Lin ◽  
Han Chang Huang ◽  
Wen Juan Liu ◽  
Zhao Feng Jiang
Keyword(s):  
Oxidative Stress ◽  
Alzheimer Disease ◽  
Mitochondrial Dysfunction ◽  
Mitochondrial Membrane ◽  
Biomedical Imaging ◽  
Chromatin Condensation ◽  
Disease Onset ◽  
Causative Role ◽  
And Oxidative Stress ◽  
Evaluating Method

Mitochondrial dysfunction and oxidative stress are among the earliest events linked to Alzheimer Disease and might play a causative role in disease onset and progression. In this paper, a biomedical imaging and visualization model was set to investigate the mitochondrial dysfunction and oxidative stress in Aβ/Cu2+-treated cells, which contribute in a significant manner to bioenergetic failure and mitochondrial dysfunction, by measuring mitochondrial membrane potential, Ca2+, chromatin condensation and ROS. This evaluating method opens a window for analyzing the protective effect of a certain substance in improving mitochondrial function and preventing oxidative stress in AD development.

Programmed cell death during microgenesis in a Honglian CMS line of rice is correlated with oxidative stress in mitochondria

2004 ◽  
Vol 31 (4) ◽  
pp. 369 ◽  
Author(s):  
Shaoqing Li ◽  
Cuixiang Wan ◽  
Jin Kong ◽  
Zaijun Zhang ◽  
Yangsheng Li ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Programmed Cell Death ◽  
Oryza Sativa L ◽  
Inner Mitochondrial Membrane ◽  
Pollen Abortion ◽  
Chronic Oxidative Stress ◽  
Excess Production ◽  
Cms Line ◽  
And Oxidative Stress

The key role of mitochondria in the integration of apoptosis and oxidative stress in mammals has been documented. In plants, mitochondria are implicated in cytoplasmic male sterility (CMS), programmed cell death (PCD), and oxidative stress. However, to date there has been no evidence presented of the interplay among CMS, PCD and oxidative stress. In this study, we demonstrate that the pollen abortion of Honglian CMS line of rice (Oryza sativa L.) displays a PCD phenotype. A premature loss of microspores was accompanied by several biochemical markers of apoptosis. Analysis of mitochondria revealed that during the PCD process there was disruption of the inner mitochondrial membrane potential in microspores. This disruption was correlated with excess production of reactive oxygen species and down-regulation of the activity of superoxide dismutase (SOD), ascorbate peroxidase (APX) and catalase in mitochondria. The excess accumulation of ROS spanned three stages from pollen mother cell to early-uninucleate stage, and was followed by the occurrence of PCD at meiosis. Our data suggest that the microspores suffered from severe oxidative stress during pollen development. It is likely the chronic oxidative stress triggered the tissue-specific PCD and consequently resulted in the abortion of microspores.

scholarly journals The anti-cancer agent guttiferone-A permeabilizes mitochondrial membrane: Ensuing energetic and oxidative stress implications

2011 ◽  
Vol 253 (3) ◽  
pp. 282-289 ◽  
Author(s):  
Gilberto L. Pardo-Andreu ◽  
Yanier Nuñez-Figueredo ◽  
Valeria G. Tudella ◽  
Osmany Cuesta-Rubio ◽  
Fernando P. Rodrigues ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Membrane ◽  
Anti Cancer ◽  
Cancer Agent ◽  
And Oxidative Stress

scholarly journals Dracocephalum moldavica L. Extracts Protect H9c2 Cardiomyocytes against H2O2-Induced Apoptosis and Oxidative Stress

2020 ◽  
Vol 2020 ◽  
pp. 1-12
Author(s):  
Min Jin ◽  
Hui Yu ◽  
Xia Jin ◽  
Lailai Yan ◽  
Jingyu Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Membrane Potential ◽  
Mitochondrial Membrane ◽  
Caspase 3 ◽  
Ethanol Extract ◽  
H9c2 Cells ◽  
Etoac Fraction ◽  
Induced Apoptosis ◽  
Phenolic And Flavonoid ◽  
And Oxidative Stress

Background and Objectives. Dracocephalum moldavica L. is an herbal medicine used to treat cardiovascular diseases in China. The purpose of this study was to assess the cardioprotective effect of D. moldavica L. extracts against H2O2-induced apoptosis and oxidative stress in H9c2 cells and to explore the mechanism behind this effect. Materials and Methods. The petroleum ether (petrol), dichloromethane (CH2Cl2), ethyl acetate (EtOAc), and n-butyl alcohol (n-BuOH) fractions were isolated from alcohol extracts of D. moldavica L. Total phenolic and flavonoid contents and in vitro antioxidant activities of different fractions were evaluated. H9c2 cells were then treated with D. moldavica L. extracts before challenging with H2O2. Cell viability was determined by colorimetric assay, and ELISA was used to measure the levels of lactate dehydrogenase (LDH), malondialdehyde (MDA), and superoxide dismutase (SOD). Apoptosis levels and mitochondrial membrane potential were measured by flow cytometry. The expressions of cell apoptosis regulatory proteins caspase-3, Bax, and Bcl-2 were determined by western blotting. Results. Our results demonstrated that the EtOAc fraction from D. moldavica L. ethanol extract, which is rich in phenolic and flavonoid active constituents, had the strongest free radical scavenging activity. Additionally, this fraction increased H2O2-induced reduction in cell viability, SOD activity, and mitochondrial membrane potential. It also reduced H2O2-induced elevation in ROS production, contents of LDH and MDA, and H9c2 apoptosis. We further found that the EtOAc fraction increased Bcl-2 expression, while it decreased caspase-3 and Bax expressions induced by H2O2 in H9c2 cells. Conclusions. Our data revealed that the EtOAc fraction from D. moldavica L. ethanol extract ameliorates H2O2-induced cardiotoxicity via antiapoptotic and antioxidant mechanisms.

scholarly journals Improving the effect of incubation and oxidative stress on thawed spermatozoa from red deer by using different antioxidant treatments

2010 ◽  
Vol 22 (5) ◽  
pp. 856 ◽  
Author(s):  
Álvaro E. Domínguez-Rebolledo ◽  
María R. Fernández-Santos ◽  
Alfonso Bisbal ◽  
José Luis Ros-Santaella ◽  
Manuel Ramón ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Lipoic Acid ◽  
Mitochondrial Membrane ◽  
Red Deer ◽  
Intracellular Reactive Oxygen Species ◽  
Oxygen Species ◽  
Positive Effects ◽  
High Concentrations ◽  
And Oxidative Stress

Antioxidants could improve sperm media, extending the viability of spermatozoa and protecting their DNA. The protective ability of lipoic acid, melatonin, Trolox and crocin was tested on red deer spermatozoa incubated at 37°C. Cryopreserved spermatozoa were thawed and incubated with 1 mM or 0.1 mM of each antioxidant, with or without oxidative stress (100 μM Fe2+). Motility (CASA), viability, mitochondrial membrane potential and acrosomal status were assessed. Lipoperoxidation (malondialdehyde production), intracellular reactive oxygen species (ROS) and DNA status (TUNEL) were checked at 4 h. Incubation alone increased ROS and decreased motility. Oxidative stress intensified these effects, increasing lipoperoxidation and DNA damage. Lipoic acid had little protective effect, whereas 1 mM melatonin showed limited protection. Trolox lowered ROS and lipoperoxidation both in oxidised and non-oxidised samples. In oxidised samples, Trolox prevented DNA and acrosomal damage, and ameliorated motility. Crocin at 1 mM showed similar results to Trolox, but noticeably stimulated motility and had no effect on lipoperoxidation. In a second experiment, a broader range of crocin and melatonin concentrations were tested, confirming the effects of crocin (positive effects noticeable at 0.5–0.75 mM), but showing an increase in lipoperoxidation at 2 mM. Melatonin was increasingly effective at 2.5 and 5 mM (ROS, lipoperoxidation and DNA status). Crocin seems a promising new antioxidant, but its particular effects on sperm physiology must be further studied, especially the consequences of motility stimulation and confirming its effect on lipoperoxidation. Melatonin might be useful at relatively high concentrations, compared to Trolox.

scholarly journals Effects of Genistein on Differentiation and Viability of Human Visceral Adipocytes

Nutrients ◽  
2018 ◽  
Vol 10 (8) ◽  
pp. 978 ◽  
Author(s):  
Elena Grossini ◽  
Serena Farruggio ◽  
Giulia Raina ◽  
David Mary ◽  
Giacomo Deiro ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Membrane Potential ◽  
Cell Viability ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Antioxidant Properties ◽  
Potential Candidate ◽  
Brown Adipocytes ◽  
Protein Activation ◽  
And Oxidative Stress

Obesity can lead to pathological growth of adipocytes by inducing inflammation and oxidative stress. Genistein could be a potential candidate for the treatment of obesity due to its antioxidant properties. Specific kits were used to examine the effects of genistein vs adiponectin on human visceral pre-adipocytes differentiation, cell viability, mitochondrial membrane potential, and oxidative stress in pre-adipocytes and in white/brown adipocytes. Western Blot was performed to examine changes in protein activation/expression. Genistein increased human visceral pre-adipocytes differentiation and browning, and caused a dose-related improvement of cell viability and mitochondrial membrane potential. Similar effects were observed in brown adipocytes and in white adipocytes, although in white cells the increase of cell viability was inversely related to the dose. Moreover, genistein potentiated AMP-activated protein kinase (AMPK)/mitofusin2 activation/expression in pre-adipocytes and white/brown adipocytes and protected them from the effects of hydrogen peroxide. The effects caused by genistein were similar to those of adiponectin. The results obtained showed that genistein increases human visceral pre-adipocytes differentiation and browning, protected against oxidative stress in pre-adipocytes and white/brown adipocytes through mechanisms related to AMPK-signalling and the keeping of mitochondrial function.

scholarly journals Mulberry Fruit Extract Affords Protection against Ethyl Carbamate-Induced Cytotoxicity and Oxidative Stress

2017 ◽  
Vol 2017 ◽  
pp. 1-12 ◽  
Author(s):  
Wei Chen ◽  
Yuting Li ◽  
Tao Bao ◽  
Vemana Gowd
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Membrane ◽  
Ethyl Carbamate ◽  
Total Phenolic ◽  
Composition Analysis ◽  
Fruit Extract ◽  
Membrane Function ◽  
Mulberry Fruit ◽  
Wide Range ◽  
And Oxidative Stress

Ethyl carbamate (EC) is a food and environmental toxicant and is a cause of concern for human exposure. Several studies indicated that EC-induced toxicity was associated with oxidative stress. Mulberry fruits are reported to have a wide range of bioactive compounds and pharmacological activities. The present study was therefore aimed to investigate the protective property of mulberry fruit extract (MFE) on EC-induced cytotoxicity and oxidative stress. Chemical composition analysis showed that total phenolic content and total flavonoid content in MFE were 502.43 ± 5.10 and 219.12 ± 4.45 mg QE/100 g FW. Cyanidin-3-O-glucoside and cyanidin-3-O-rutinoside were the major anthocyanins in MFE. In vitro antioxidant studies (DPPH, ABTS, and FRAP assays) jointly exhibited the potent antioxidant capacity of MFE. Further study indicated that MFE protected human liver HepG2 cells from EC-induced cytotoxicity by scavenging overproduced cellular ROS. EC treatment promoted intracellular glutathione (GSH) depletion and caused mitochondrial membrane potential (MMP) collapse, as well as mitochondrial membrane lipid peroxidation, whereas MFE pretreatment significantly inhibited GSH depletion and restored the mitochondrial membrane function. Overall, our study suggested that polyphenolic-rich MFE could afford a potent protection against EC-induced cytotoxicity and oxidative stress.

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