NARP mutation and mtDNA depletion trigger mitochondrial biogenesis which can be modulated by selenite supplementation

Wojewoda, Marta; Duszyński, Jerzy; Szczepanowska, Joanna

doi:10.1016/j.biocel.2011.04.011

Cited by 25 publications

(17 citation statements)

References 45 publications

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“…Of course, this mechanism would only control a fraction of the total complement of mitochondrial proteins, thereby leading to altered organelle composition, and possible dysfunction. As is often the case in the existence of dysfunctional mitochondria, such as in mitochondrial disease, a compensatory upregulation of mitochondrial content can be evident (21,39,46), as our data suggest. To fulfill our second purpose, we analyzed the effects of contractile activity on the components identified to be required for the mTORC1 transcriptional complex, including PGC-1␣, raptor, phospho-mTOR (Ser 2448 ), and YY1.…”

Section: Discussionsupporting

confidence: 83%

Contractile activity-induced mitochondrial biogenesis and mTORC1

Carter

Hood

2012

American Journal of Physiology-Cell Physiology

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Section: Discussionsupporting

confidence: 83%

Contractile activity-induced mitochondrial biogenesis and mTORC1

Carter

Hood

2012

American Journal of Physiology-Cell Physiology

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“…Treatment of cells with Selol followed by SNP exposure resulted in the increase of target genes expression, thus it is likely that Nrf2 mediates the observed effects. It corresponds with a report where selenite induced protective changes in mitochondrial biogenesis by increasing the level of Nrf1 and nuclear accumulation of Nrf2 [61]. …”

Section: Discussionsupporting

confidence: 91%

Protective Effects of Selol Against Sodium Nitroprusside-Induced Cell Death and Oxidative Stress in PC12 Cells

et al. 2016

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Selol is an organic selenitetriglyceride formulation containing selenium at +4 oxidation level that can be effectively incorporated into catalytic sites of of Se-dependent antioxidants. In the present study, the potential antioxidative and cytoprotective effects of Selol against sodium nitroprusside (SNP)-evoked oxidative/nitrosative stress were investigated in PC12 cells and the underlying mechanisms analyzed. Spectrophoto- and spectrofluorimetic methods as well as fluorescence microscopy were used in this study; mRNA expression was quantified by real-time PCR. Selol dose-dependently improved the survival and decreased the percentage of apoptosis in PC12 cells exposed to SNP. To determine the mechanism of this protective action, the effect of Selol on free radical generation and on antioxidative potential was evaluated. Selol offered significant protection against the elevation of reactive oxidative species (ROS) evoked by SNP. Moreover, this compound restored glutathione homeostasis by ameliorating the SNP-evoked disturbance of GSH/GSSG ratio. The protective effect exerted by Selol was associated with the prevention of SNP-mediated down-regulation of antioxidative enzymes: glutathione peroxidase (Se-GPx), glutathione reductase (GR), and thioredoxin reductase (TrxR). Finally, GPx inhibition significantly abolished the cytoprotective effect of Selol. In conclusion, these results suggest that Selol effectively protected PC12 cells against SNP-induced oxidative damage and death by adjusting free radical levels and antioxidant system, and suppressing apoptosis. Selol could be successfully used in the treatments of diseases that involve oxidative stress and resulting apoptosis.

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“…Selenium has traditionally been used as a supplement for several decades in the prevention and treatment of human diseases including Keshan cardiomyopathy [25], Kashin-Beck osteoarthropathy [26, 27], osteopenia [28] and certain forms of cancers [29–31], and has been shown to modulate the functions of a variety of intracellular proteins [32–34]. Recent research has focused on the neuroprotective potential of selenium as a candidate for therapeutic intervention in hypoxic injuries and ischemia-induced neuronal damage [35–39].…”

Section: Discussionmentioning

confidence: 99%

Selenium suppresses glutamate-induced cell death and prevents mitochondrial morphological dynamic alterations in hippocampal HT22 neuronal cells

Ibeanu

Wang

et al. 2017

BMC Neurosci

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BackgroundPrevious studies have indicated that selenium supplementation may be beneficial in neuroprotection against glutamate-induced cell damage, in which mitochondrial dysfunction is considered a major pathogenic feature. However, the exact mechanisms by which selenium protects against glutamate-provoked mitochondrial perturbation remain ambiguous. In this study glutamate exposed murine hippocampal neuronal HT22 cell was used as a model to investigate the underlying mechanisms of selenium-dependent protection against mitochondria damage.ResultsWe find that glutamate-induced cytotoxicity was associated with enhancement of superoxide production, activation of caspase-9 and -3, increases of mitochondrial fission marker and mitochondrial morphological changes. Selenium significantly resolved the glutamate-induced mitochondria structural damage, alleviated oxidative stress, decreased Apaf-1, caspases-9 and -3 contents, and altered the autophagy process as observed by a decline in the ratio of the autophagy markers LC3-I and LC3-II.ConclusionThese findings suggest that the protection of selenium against glutamate stimulated cell damage of HT22 cells is associated with amelioration of mitochondrial dynamic imbalance.

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NARP mutation and mtDNA depletion trigger mitochondrial biogenesis which can be modulated by selenite supplementation

Cited by 25 publications

References 45 publications

Contractile activity-induced mitochondrial biogenesis and mTORC1

Contractile activity-induced mitochondrial biogenesis and mTORC1

Protective Effects of Selol Against Sodium Nitroprusside-Induced Cell Death and Oxidative Stress in PC12 Cells

Selenium suppresses glutamate-induced cell death and prevents mitochondrial morphological dynamic alterations in hippocampal HT22 neuronal cells

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