scholarly journals Humic Substances Mitigate the Impact of Tritium on Luminous Marine Bacteria. Involvement of Reactive Oxygen Species

2020 ◽  
Vol 21 (18) ◽  
pp. 6783 ◽  
Author(s):  
Tatiana V. Rozhko ◽  
Olga V. Kolesnik ◽  
Gennadii A. Badun ◽  
Devard I. Stom ◽  
Nadezhda S. Kudryasheva
Keyword(s):  
Reactive Oxygen Species ◽  
Humic Substances ◽  
Marine Bacteria ◽  
Low Dose ◽  
Tritiated Water ◽  
Reactive Oxygen ◽  
Physiological Parameter ◽  
Oxygen Species ◽  
Luminous Bacteria ◽  
The Impact

The paper studies the combined effects of beta-emitting radionuclide tritium and Humic Substances (HS) on the marine unicellular microorganism—luminous bacteria—under conditions of low-dose radiation exposures (<0.04 Gy). Tritium was used as a component of tritiated water. Bacterial luminescence intensity was considered as a tested physiological parameter. The bioluminescence response of the marine bacteria to tritium corresponded to the “hormesis” model: it included stages of bioluminescence inhibition and activation, as well as the absence of the effect. HS were shown to decrease the inhibition and activation effects of tritium, similar to those of americium-241, alpha-emitting radionuclide, studied earlier. Correlations between the bioluminescence intensity and the content of Reactive Oxygen Species (ROS) were found in the radioactive bacterial suspensions. The results demonstrate an important role of HS in natural processes in the regions of low radioactive contamination: HS can mitigate radiotoxic effects and adaptive response of microorganisms to low-dose radioactive exposures. The involvement of ROS in these processes was demonstrated.

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 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.

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.

The impact of mitochondria and reactive oxygen species on the proliferation of human amniotic mesenchymal stromal cells

2018 ◽  
Vol 1859 ◽  
pp. e45
Author(s):  
Sergiu Dumitrescu ◽  
Adelheid Weidinger ◽  
Asmita Banerjee ◽  
Susanne Wolbank ◽  
Karlheinz Hilber ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Mesenchymal Stromal Cells ◽  
Stromal Cells ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
The Impact

scholarly journals The impact of dehydration rate on the production and cellular location of reactive oxygen species in an aquatic moss

2012 ◽  
Vol 110 (5) ◽  
pp. 1007-1016 ◽  
Author(s):  
Ricardo Cruz de Carvalho ◽  
Myriam Catalá ◽  
Jorge Marques da Silva ◽  
Cristina Branquinho ◽  
Eva Barreno
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Aquatic Moss ◽  
Cellular Location ◽  
Dehydration Rate ◽  
The Impact

scholarly journals The Neuro-Protective Effects of the TSPO Ligands CB86 and CB204 on 6-OHDA-Induced PC12 Cell Death as an In Vitro Model for Parkinson’s Disease

Biology ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 1183
Author(s):  
Sheelu Monga ◽  
Nunzio Denora ◽  
Valentino Laquintana ◽  
Rami Yashaev ◽  
Abraham Weizman ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Cell Death ◽  
Neurodegenerative Disorder ◽  
Reactive Oxygen ◽  
Ros Generation ◽  
Oxygen Species ◽  
The Impact

Parkinson’s disease (PD) is a progressive neurodegenerative disorder which is characterized by the degeneration of dopaminergic neurons in substantia nigra (SN). Oxidative stress or reactive oxygen species (ROS) generation was suggested to play a role in this specific type of neurodegeneration. Therapeutic options which can target and counteract ROS generation may be of benefit. TSPO ligands are known to counteract with neuro-inflammation, ROS generation, apoptosis, and necrosis. In the current study, we investigated an in vitro cellular PD model by the assessment of 6-hydroxydopamine (6-OHDA, 80 µM)-induced PC12 neurotoxicity. Simultaneously to the exposure of the cells to 6-OHDA, we added the TSPO ligands CB86 and CB204 (25 µM each) and assessed the impact on several markers of cell death. The two ligands normalized significantly (57% and 52% respectively, from 44%; whereas the control was 68%) cell proliferation at different time points from 0–24 h. Additionally, we evaluated the effect of these two TSPO ligands on necrosis using propidium iodide (PI) staining and found that the ligands inhibited significantly the 6-OHDA-induced necrosis. As compared to control, the red count was increased up to 57-fold whereas CB86 and CB204 inhibited to 2.7-fold and 3.2-fold respectively. Necrosis was also analyzed by LDH assay which showed significant effect. Both assays demonstrated similar potent anti-necrotic effect of the two TSPO ligands. Reactive oxygen species (ROS) generation induced by 6-OHDA was also inhibited by the two TSPO ligand up to 1.3 and 1.5-fold respectively, as compared to 6-OHDA group. CB86 and CB204 inhibited also normalized the cell viability up to 1.8-fold after the exposure to 6-OHDA, as assessed by XTT assay. The two TSPO ligands also inhibited apoptosis significantly (1.3-fold for both) as assessed by apopxin green staining. In summary, it appears that the two TSPO ligands CB86 and CB204 can suppress cell death of PC12 induced by 6-OHDA. The results may be relevant to the use of these two TSPO ligands as therapeutic option neurodegenerative diseases like PD.

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