High doses of sodium tungstate can promote mitochondrial dysfunction and oxidative stress in isolated mitochondria

Cheraghi, Ghazale; Hajiabedi, Elnaz; Niaghi, Behnaz; Nazari, Firouzeh; Naserzadeh, Parvaneh; Hosseini, Mir-Jamal

doi:10.1002/jbt.22266

Cited by 23 publications

(11 citation statements)

References 29 publications

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“…The level of ROS was measured by flow cytometry and DCFH‐DA as reagent as described in the authors’ previous study (Cheraghi et al., 2019). In flow cytograms, nontreated isolated cells (control) showed relatively weak fluorescence signal because of self‐quenching.…”

Section: Resultsmentioning

confidence: 99%

“…Reduced GSH level as a strong antioxidant system protected cells from damaging effects of ROS formation and oxidized GSH (Pourahmad et al., 2011). Lack of balance between oxidants and antioxidants levels led to oxidative damages in lipids, proteins and nucleic acids caused to initiation of cell death signaling (Cheraghi et al., 2019). Although ROS level increased after exposure to 3‐MCPD, no decrease in the GSH level was observed on different concentration of 3‐MCPD (except for 10 µM) in isolated kidney cells.…”

Section: Resultsmentioning

confidence: 99%

“…In the next step, to decrease the activation of damaging phospholipases and proteases to its minimum level, homogenization was done in cold mannitol solution at 4 °C. Then, the homogenate was centrifuged (1,000 × g , 10 min at 4 °C) and the obtained supernatant was centrifuged again (10,000 × g , 10 min, at 4 °C) as a source of mitochondrial fraction according to the authors’ previous study (Cheraghi et al., 2019). The obtained pellet (P 2 fraction) including synaptic and nonsynaptic mitochondria was resuspended in the Tris buffer that contained 0.05 M Tris‐HCl, 0.25 M sucrose, 20 mM KCl, 2.0 mM MgCl 2 , and 1.0 mM Na 2 HPO 4 (pH 7.4 at 4 °C.…”

Section: Methodsmentioning

confidence: 99%

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Toxicological assessment of 3‐monochloropropane‐1,2‐diol (3‐MCPD) as a main contaminant of foodstuff in three different in vitro models: Involvement of oxidative stress and cell death signaling pathway

Nazari

Naserzadeh

Dizaji

et al. 2020

Journal of Food Science

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3‐Monochloropropane‐1,2‐diol (3‐MCPD) as a main source of food contamination has always been known as a carcinogenic agent. Kidney, liver, testis, and heart seem to be the main target organs for 3‐MCPD. Because oxidative stress and mitochondrial dysfunction have been realized to be involved in 3‐MCPD‐induced cytotoxicity, the present study aimed to investigate the probable toxicity mechanisms of 3‐MCPD in isolated mitochondria, HEK‐293 cell line, and cell isolated from the rats’ liver and kidney through measuring multiparametric oxidative stress assay. Based on the data indicating no significant difference between 3‐MCPD‐treated groups and control group, metabolites of 3‐MCPD have a key role in organ toxicity caused by them. To further investigating the suggested hypothesis, the effect of 3‐MCPD toxicity on HEK‐293 cell line was examined. Although the proliferation declined after exposure to a low dose of 3‐MCPD (10 to 200 µM), controversial responses in higher concentration (2 to 10 mM) have led to studies on the effect of oxidative stress and cell death signaling on isolated kidney and liver cells. Treatment of the isolated kidney and liver cells with 3‐MCPD resulted in an increase in the level of reactive oxygen species (ROS), the collapse of mitochondrial membrane potential (MMP), and activation of cell death signaling without creating any significant difference in the amount of reduced glutathione. In fact, 3‐MCPD can disrupt the mitochondrial electron transfer in isolated cells, which is correlated with the impairment of mitochondrial oxidative phosphorylation system, the rise of ROS level, and the failure of MMP, leading to the release of cytochrome c from mitochondria to cytosol and finally the activation of cell death signaling.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

See 1 more Smart Citation

Toxicological assessment of 3‐monochloropropane‐1,2‐diol (3‐MCPD) as a main contaminant of foodstuff in three different in vitro models: Involvement of oxidative stress and cell death signaling pathway

Nazari

Naserzadeh

Dizaji

et al. 2020

Journal of Food Science

Self Cite

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“…Oxidative stress causes damage to cell components, especially mitochondria, which are the site of ROS production and also the target of oxidative stress-induced damage [8]; previous reports have shown that ROS accumulation induced the mitochondrial respiratory chain damage [4]. Excessive uorine intake increases the accumulation of ROS in the liver, suggesting that uorine destroys the mitochondrial respiratory chain, which is mainly characterized by the occurrence of oxidative stress and the decrease of ATP content [33].…”

Section: Discussionmentioning

confidence: 99%

Ameliorative Effects of Nano-Selenium Against Fluoride Stress Induced Hepatocytes Autophagy and Apoptosis in Mice

Wang

Liu

Han

et al. 2020

Preprint

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Background: Fluorine is widespread in the environment, and the injurious impacts of fluoride underscore its significance for public health. The long-term presence of fluorine in environment could be a risk in hepatotoxicity for both human beings and animals. Important role of selenium in mitigation of heavy metal toxicity via regulating autophagy and apoptosis is well-known. Further, nano-Se is a common artificial nano material, with higher biological activity and lower toxicity. The aim of the current study was to examine whether nano-Se supplementation can reduce the effects of fluoride-induced hepatocytes autophagy and apoptosis. Results: Here, we report that fluoride exposure induces apoptosis and autophagy with nucleus broken, dissolved and disappeared of hepatocyte, contributing to its hepatotoxicity. More importantly, Cyt-C and Beclin-1/Bcl-2 pathways are involved in the regulation of autophagy and apoptosis via targeting Caspase-9, Caspase-3, P53, Bax, LC3, ATG-5, P62 and mTOR expressions. Conclusion: Nano-Se is capable to alleviate fluoride-induced hepatocyte damage, that selenium can be prefer to prevent chronic fluorosis-induced autophagy and apoptosis by regulating Cyt-C and Beclin-1/Bcl-2 signaling pathway. In precisely, NaF-induced the liver injury by activating autophagy and apoptosis, which indicate that fluorine exposure, pose an ecological risk to human beings and animals. Nano-Se has protective effects against fluoride-induced hepatocytes.

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“…АФК выступают в роли стрессового фактора на энергетическом уровне клетки. Это приводит к снижению АТФ, что приводит к усиленному синтезу АТФ и снижению электрохимического градиента [18].…”

Section: обсуждение полученных результатовunclassified

Dynamics of Mitochondrial Transmembrane Potential Changes in Blood Monocytes in Conditions of Development and Course of Experimental Periodontitis and the Effect of Korvityn on it

Demkovych¹,

Machogan²

2020

Ukr. ž. med. bìol. sportu

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Inflammatory diseases of periodontal tissues remain one of the most complex and unresolved problems of modern dentistry. The most important internal stimulus for triggering apoptosis is DNA damage in response to various factors (including reactive oxygen species). Mitochondrial transmembrane potential (Δψm) is generated by the electrochemical gradient of protons on both sides of the membrane and is closely related to the functioning of mitochondria, its support is provided by the processes of electron transfer in the respiratory chain. The purpose of our study was to elucidate the pathogenetic role of changes in mitochondrial transmebranic potential in the dynamics of the inflammatory response in experimental bacterial-immune periodontitis and the effects of quercetin (Korvityn) on it. Material and methods. The study was performed on white clinically healthy rats. Experimental bacterial-immune periodontitis in experimental animals was induced by injection of a mixture of microorganisms diluted with egg protein into the tissues of the periodontal complex. Quercetin was administered by intramuscular injection for correction. Evaluation of changes in mitochondrial transmembrane potential of leukocytes was performed by flow cytofluorimetry. Results and discussion. In experimental bacterial-immune periodontitis, the percentage of cells with reduced mitochondrial transmembrane potential among blood monocytes significantly increased. In animals on the 7th day of the study, the number of cells with reduced mitochondrial transmembrane potential among blood monocytes increased significantly compared with the control group. For the next study period (14th day), the number of cells with reduced ∆ψm decreased compared to the 7th day of the experiment. Having analyzed the data of mitochondrial transmembrane potential of blood monocytes on the 30th day of the experiment, we noted that they decreased relative to those obtained on the 14th day of the study, indicating profound oxidative imbalance in cells and destabilization of the mitochondrial membrane. The use of quercetin led to a decrease in the values compared to the data of animals with our simulated pathology on the 14th day, the experiment without the introduction of flavonol, but they remained significantly higher than the control group of animals. Conclusion. Flavonol (Korvityn) quercetin reduced mitochondrial transmembrane potential in experimental bacterial-immune periodontitis, which was evidence by stabilization and attenuation of the inflammatory process

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High doses of sodium tungstate can promote mitochondrial dysfunction and oxidative stress in isolated mitochondria

Cited by 23 publications

References 29 publications

Toxicological assessment of 3‐monochloropropane‐1,2‐diol (3‐MCPD) as a main contaminant of foodstuff in three different in vitro models: Involvement of oxidative stress and cell death signaling pathway

Toxicological assessment of 3‐monochloropropane‐1,2‐diol (3‐MCPD) as a main contaminant of foodstuff in three different in vitro models: Involvement of oxidative stress and cell death signaling pathway

Ameliorative Effects of Nano-Selenium Against Fluoride Stress Induced Hepatocytes Autophagy and Apoptosis in Mice

Dynamics of Mitochondrial Transmembrane Potential Changes in Blood Monocytes in Conditions of Development and Course of Experimental Periodontitis and the Effect of Korvityn on it

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