scholarly journals Corrigendum to “Kinetic Modeling of the Mitochondrial Energy Metabolism of Neuronal Cells: The Impact of Reduced α-Ketoglutarate Dehydrogenase Activities on ATP Production and Generation of Reactive Oxygen Species”

2018 ◽  
Vol 2018 ◽  
pp. 1-2
Author(s):  
Nikolaus Berndt ◽  
Sascha Bulik ◽  
Hermann-Georg Holzhütter
Keyword(s):  
Reactive Oxygen Species ◽  
Energy Metabolism ◽  
Kinetic Modeling ◽  
Neuronal Cells ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Mitochondrial Energy Metabolism ◽  
Atp Production ◽  
The Impact ◽  
Ketoglutarate Dehydrogenase

scholarly journals Kinetic Modeling of the Mitochondrial Energy Metabolism of Neuronal Cells: The Impact of Reducedα-Ketoglutarate Dehydrogenase Activities on ATP Production and Generation of Reactive Oxygen Species

2012 ◽  
Vol 2012 ◽  
pp. 1-11 ◽  
Author(s):  
Nikolaus Berndt ◽  
Sascha Bulik ◽  
Hermann-Georg Holzhütter
Keyword(s):  
Reactive Oxygen Species ◽  
Neurodegenerative Diseases ◽  
Neuronal Cells ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Mitochondrial Energy Metabolism ◽  
Atp Production ◽  
Dependent Inactivation ◽  
The Impact ◽  
Ketoglutarate Dehydrogenase

Reduced activity of brain α-ketoglutarate dehydrogenase complex (KGDHC) occurs in a number of neurodegenerative diseases like Parkinson's disease and Alzheimer's disease. In order to quantify the relation between diminished KGDHC activity and the mitochondrial ATP generation, redox state, transmembrane potential, and generation of reactive oxygen species (ROS) by the respiratory chain (RC), we developed a detailed kinetic model. Model simulations revealed a threshold-like decline of the ATP production rate at about 60% inhibition of KGDHC accompanied by a significant increase of the mitochondrial membrane potential. By contrast, progressive inhibition of the enzyme aconitase had only little impact on these mitochondrial parameters. As KGDHC is susceptible to ROS-dependent inactivation, we also investigated the reduction state of those sites of the RC proposed to be involved in ROS production. The reduction state of all sites except one decreased with increasing degree of KGDHC inhibition suggesting an ROS-reducing effect of KGDHC inhibition. Our model underpins the important role of reduced KGDHC activity in the energetic breakdown of neuronal cells during development of neurodegenerative diseases.

scholarly journals Mitochondrial Reactive Oxygen Species (ROS) Production Alters Sperm Quality

Antioxidants ◽  
2021 ◽  
Vol 10 (1) ◽  
pp. 92
Author(s):  
Rosanna Chianese ◽  
Riccardo Pierantoni
Keyword(s):  
Reactive Oxygen Species ◽  
Sperm Quality ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Cellular Functions ◽  
Apoptotic Pathway ◽  
Atp Production ◽  
Mammalian Sperm ◽  
Offspring Health ◽  
The Impact

Besides ATP production, mitochondria are key organelles in several cellular functions, such as steroid hormone biosynthesis, calcium homoeostasis, intrinsic apoptotic pathway, and the generation of reactive oxygen species (ROS). Despite the loss of the majority of the cytoplasm occurring during spermiogenesis, mammalian sperm preserves a number of mitochondria that rearrange in a tubular structure at the level of the sperm flagellum midpiece. Although sperm mitochondria are destroyed inside the zygote, the integrity and the functionality of these organelles seem to be critical for fertilization and embryo development. The aim of this review was to discuss the impact of mitochondria-produced ROS at multiple levels in sperm: the genome, proteome, lipidome, epigenome. How diet, aging and environmental pollution may affect sperm quality and offspring health—by exacerbating oxidative stress—will be also described.

scholarly journals Assessment of Physico-Chemical and Toxicological Properties of Commercial 2D Boron Nitride Nanopowder and Nanoplatelets

2021 ◽  
Vol 22 (2) ◽  
pp. 567
Author(s):  
Brixhilda Domi ◽  
Kapil Bhorkar ◽  
Carlos Rumbo ◽  
Labrini Sygellou ◽  
Spyros N. Yannopoulos ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Boron Nitride ◽  
A549 Cells ◽  
Reactive Oxygen ◽  
Slight Reduction ◽  
Oxygen Species ◽  
Potential Toxicity ◽  
Cellular Models ◽  
Physico Chemical ◽  
The Impact

Boron nitride (BN) nanomaterials have been increasingly explored for potential applications in chemistry and biology fields (e.g., biomedical, pharmaceutical, and energy industries) due to their unique physico-chemical properties. However, their safe utilization requires a profound knowledge on their potential toxicological and environmental impact. To date, BN nanoparticles have been considered to have a high biocompatibility degree, but in some cases, contradictory results on their potential toxicity have been reported. Therefore, in the present study, we assessed two commercial 2D BN samples, namely BN-nanopowder (BN-PW) and BN-nanoplatelet (BN-PL), with the objective to identify whether distinct physico-chemical features may have an influence on the biological responses of exposed cellular models. Morphological, structural, and composition analyses showed that the most remarkable difference between both commercial samples was the diameter of their disk-like shape, which was of 200–300 nm for BN-PL and 100–150 nm for BN-PW. Their potential toxicity was investigated using adenocarcinomic human alveolar basal epithelial cells (A549 cells) and the unicellular fungus Saccharomycescerevisiae, as human and environmental eukaryotic models respectively, employing in vitro assays. In both cases, cellular viability assays and reactive oxygen species (ROS) determinations where performed. The impact of the selected nanomaterials in the viability of both unicellular models was very low, with only a slight reduction of S. cerevisiae colony forming units being observed after a long exposure period (24 h) to high concentrations (800 mg/L) of both nanomaterials. Similarly, BN-PW and BN-PL showed a low capacity to induce the formation of reactive oxygen species in the studied conditions. Even at the highest concentration and exposure times, no major cytotoxicity indicators were observed in human cells and yeast. The results obtained in the present study provide novel insights into the safety of 2D BN nanomaterials, indicating no significant differences in the toxicological potential of similar commercial products with a distinct lateral size, which showed to be safe products in the concentrations and exposure conditions tested.

scholarly journals Role of Natural Antioxidants on Neuroprotection and Neuroinflammation

Antioxidants ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 608
Author(s):  
Domenico Nuzzo
Keyword(s):  
Reactive Oxygen Species ◽  
Energy Metabolism ◽  
Respiratory Chain ◽  
Reactive Oxygen ◽  
Natural Antioxidants ◽  
Oxygen Species

All cells continuously generate reactive oxygen species (ROS) through the respiratory chain during the energy metabolism process [...]

scholarly journals MitoQ Is Able to Modulate Apoptosis and Inflammation

2021 ◽  
Vol 22 (9) ◽  
pp. 4753
Author(s):  
Elisa Piscianz ◽  
Alessandra Tesser ◽  
Erika Rimondi ◽  
Elisabetta Melloni ◽  
Claudio Celeghini ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Mevalonate Pathway ◽  
Neuronal Cell ◽  
Reactive Oxygen ◽  
Mitochondrial Activity ◽  
Oxygen Species ◽  
Short Period ◽  
Inflammatory Stimuli ◽  
Apoptosis And Inflammation ◽  
The Impact

Mitoquinone (MitoQ) is a mitochondrial reactive oxygen species scavenger that is characterized by high bioavailability. Prior studies have demonstrated its neuroprotective potential. Indeed, the release of reactive oxygen species due to damage to mitochondrial components plays a pivotal role in the pathogenesis of several neurodegenerative diseases. The present study aimed to examine the impact of the inflammation platform activation on the neuronal cell line (DAOY) treated with specific inflammatory stimuli and whether MitoQ addition can modulate these deregulations. DAOY cells were pre-treated with MitoQ and then stimulated by a blockade of the cholesterol pathway, also called mevalonate pathway, using a statin, mimicking cholesterol deregulation, a common parameter present in some neurodegenerative and autoinflammatory diseases. To verify the role played by MitoQ, we examined the expression of genes involved in the inflammation mechanism and the mitochondrial activity at different time points. In this experimental design, MitoQ showed a protective effect against the blockade of the mevalonate pathway in a short period (12 h) but did not persist for a long time (24 and 48 h). The results obtained highlight the anti-inflammatory properties of MitoQ and open the question about its application as an effective adjuvant for the treatment of the autoinflammatory disease characterized by a cholesterol deregulation pathway that involves mitochondrial homeostasis.

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