scholarly journals Disruption of Neurotransmission, Membrane Potential, and Mitochondrial Calcium in the Brain and Spinal Cord of Nile Tilapia Elicited by Microcystis Aeruginosa Extract: An Uncommon Consequence of the Eutrophication Process

2021 ◽  
Author(s):  
Minerva Nájera-Martínez ◽  
Goretti Guadalupe Landon-Hernández ◽  
José Pablo Romero-López ◽  
María Lilia Domínguez-López ◽  
Ethel Awilda García-Latorre ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Protein Phosphatase ◽  
Nile Tilapia ◽  
Mitochondrial Membrane ◽  
Positive Control ◽  
Mitochondrial Calcium ◽  
Brain And Spinal Cord ◽  
The Brain

Abstract Microcystins (MCs) are produced during the growth and proliferation of some species of cyanobacteria, mainly Microcystis aeruginosa, which has massive growth in eutrophic water bodies. Microcystins are highly toxic Microcystis-derived metabolites that exert its main effect in the liver through the inhibition of protein phosphatase (PP1 and PP2A). However, other damages in fish species are less documented and could be unexpected. The aim of the current study was to evaluate the effects of Microcystis aeruginosa extract (MaE) into the central nervous system (CNS) of the Nile tilapia. The MaE was normalized by MCs content (MC-LR). We include a positive control for protein phosphatase inhibition, norcantharidin intraperitoneally dosed at sublethal levels. On the eighth day, measurement of neurotransmission biomarkers (AChE, BChE, CbE and GABA) were measured, as well as levels of mitochondrial calcium, and the mitochondrial membrane potential by flow cytometry in the brain and spinal cord were assessed, in addition to the PP1/PP2A activity in the liver. The MCs elicited mortality at 5 µg/L. The positive control and MCs at sublethal levels inhibited the PP1/PP2A activity in the liver and induced alterations in the neurotoxicity biomarkers evaluated in the CNS. This response is probably due to the disruption of transport ions, dependent and independent of ATP because of alterations in the mitochondrial membrane potential and mitochondrial calcium. The findings of this study suggest that pollutants capable of inducing cyanobacterial blooms are able, in an indirect way, to exert neurotoxic effects in fish species through MC levels.

scholarly journals Peroxiredoxin II Maintains the Mitochondrial Membrane Potential against Alcohol-Induced Apoptosis in HT22 Cells

Antioxidants ◽  
2019 ◽  
Vol 9 (1) ◽  
pp. 1
Author(s):  
Mei-Hua Jin ◽  
Jia-Bin Yu ◽  
Hu-Nan Sun ◽  
Ying-Hua Jin ◽  
Gui-Nan Shen ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Ht22 Cells ◽  
Apoptotic Protein ◽  
Intracellular Ros ◽  
Induced Apoptosis ◽  
The Brain

Excessive alcohol intake can significantly reduce cognitive function and cause irreversible learning and memory disorders. The brain is particularly vulnerable to alcohol-induced ROS damage; the hippocampus is one of the most sensitive areas of the brain for alcohol neurotoxicity. In the present study, we observed significant increasing of intracellular ROS accumulations in Peroxiredoxin II (Prx II) knockdown HT22 cells, which were induced by alcohol treatments. We also found that the level of ROS in mitochondrial was also increased, resulting in a decrease in the mitochondrial membrane potential. The phosphorylation of GSK3β (Ser9) and anti-apoptotic protein Bcl2 expression levels were significantly downregulated in Prx II knockdown HT22 cells, which suggests that Prx II knockdown HT22 cells were more susceptible to alcohol-induced apoptosis. Scavenging the alcohol-induced ROS with NAC significantly decreased the intracellular ROS levels, as well as the phosphorylation level of GSK3β in Prx II knockdown HT22 cells. Moreover, NAC treatment also dramatically restored the mitochondrial membrane potential and the cellular apoptosis in Prx II knockdown HT22 cells. Our findings suggest that Prx II plays a crucial role in alcohol-induced neuronal cell apoptosis by regulating the cellular ROS levels, especially through regulating the ROS-dependent mitochondrial membrane potential. Consequently, Prx II may be a therapeutic target molecule for alcohol-induced neuronal cell death, which is closely related to ROS-dependent mitochondria dysfunction.

scholarly journals Expression of the mitochondrial calcium uniporter in cardiac myocytes improves impaired mitochondrial calcium handling and metabolism in simulated hyperglycemia

2016 ◽  
Vol 311 (6) ◽  
pp. C1005-C1013 ◽  
Author(s):  
Julieta Diaz-Juarez ◽  
Jorge Suarez ◽  
Federico Cividini ◽  
Brian T. Scott ◽  
Tanja Diemer ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Membrane Potential ◽  
Cardiac Myocytes ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Calcium Handling ◽  
Acid Oxidation ◽  
Mitochondrial Calcium ◽  
Pathophysiological Mechanism ◽  
Protein Levels

Diabetic cardiomyopathy is associated with metabolic changes, including decreased glucose oxidation (Gox) and increased fatty acid oxidation (FAox), which result in cardiac energetic deficiency. Diabetic hyperglycemia is a pathophysiological mechanism that triggers multiple maladaptive phenomena. The mitochondrial Ca2+ uniporter (MCU) is the channel responsible for Ca2+ uptake in mitochondria, and free mitochondrial Ca2+ concentration ([Ca2+]m) regulates mitochondrial metabolism. Experiments with cardiac myocytes (CM) exposed to simulated hyperglycemia revealed reduced [Ca2+]m and MCU protein levels. Therefore, we investigated whether returning [Ca2+]m to normal levels in CM by MCU expression could lead to normalization of Gox and FAox with no detrimental effects. Mouse neonatal CM were exposed for 72 h to normal glucose [5.5 mM glucose + 19.5 mM mannitol (NG)], high glucose [25 mM glucose (HG)], or HG + adenoviral MCU expression. Gox and FAox, [Ca2+]m, MCU levels, pyruvate dehydrogenase (PDH) activity, oxidative stress, mitochondrial membrane potential, and apoptosis were assessed. [Ca2+]m and MCU protein levels were reduced after 72 h of HG. Gox was decreased and FAox was increased in HG, PDH activity was decreased, phosphorylated PDH levels were increased, and mitochondrial membrane potential was reduced. MCU expression returned these parameters toward NG levels. Moreover, increased oxidative stress and apoptosis were reduced in HG by MCU expression. We also observed reduced MCU protein levels and [Ca2+]m in hearts from type 1 diabetic mice. Thus we conclude that HG-induced metabolic alterations can be reversed by restoration of MCU levels, resulting in return of [Ca2+]m to normal levels.

Oxidative stress and mitochondrial membrane potential are involved in the cytotoxicity of perfluorododecanoic acid to neurons

2020 ◽  
Vol 36 (11) ◽  
pp. 892-897
Author(s):  
Xuemei Fang ◽  
Xingtao Zhang ◽  
Hongxia Li
Keyword(s):  
Oxidative Stress ◽  
Membrane Potential ◽  
Pc12 Cells ◽  
Mitochondrial Membrane Potential ◽  
Cognitive Deficits ◽  
Mitochondrial Membrane ◽  
Caspase 3 ◽  
Oxygen Species ◽  
Total Antioxidant ◽  
The Brain

Perfluorododecanoic acid (PFDoA), used in numerous commercial products, was recently demonstrated to accumulate in the brain more easily than other perfluorinated compounds and to cause cognitive deficits. In this study, pheochromocytoma 12 (PC12) cells were exposed to doses of PFDoA to explore the cytotoxicity of this compound to neurons. The results showed that treatment with PFDoA decreased PC12 cell viability dose-dependently. Treatment with 50 and 100 µM PFDoA significantly increased reactive oxygen species ( p < 0.01) and malondialdehyde ( p < 0.01) and decreased total antioxidant capacity ( p < 0.05 and p < 0.01, respectively) in PC12 cells. The administration of 50 and 100 µM PFDoA led to a loss of mitochondrial membrane potential (MMP) ( p < 0.05 and p < 0.01, respectively) in PC12 cells. The activity of caspase 3 was obviously increased ( p < 0.05) in 100 µM PFDoA-treated PC12 cells. In general, the results demonstrated that PFDoA exposure could result in the disruption of MMP, which may contribute to the increase of oxidative stress and activation of the apoptotic signaling cascade in PC12 cells.

scholarly journals Mitochondrial Dysfunction in Chronic Respiratory Diseases: Implications for the Pathogenesis and Potential Therapeutics

2021 ◽  
Vol 2021 ◽  
pp. 1-20
Author(s):  
Wen-cheng Zhou ◽  
Jiao Qu ◽  
Sheng-yang Xie ◽  
Yang Sun ◽  
Hong-wei Yao
Keyword(s):  
Mitochondrial Dna ◽  
Membrane Potential ◽  
Mitochondrial Dysfunction ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Respiratory Diseases ◽  
Metabolic Reprogramming ◽  
Mitochondrial Calcium ◽  
Chronic Respiratory Diseases ◽  
Cellular Processes

Mitochondria are indispensable for energy metabolism and cell signaling. Mitochondrial homeostasis is sustained with stabilization of mitochondrial membrane potential, balance of mitochondrial calcium, integrity of mitochondrial DNA, and timely clearance of damaged mitochondria via mitophagy. Mitochondrial dysfunction is featured by increased generation of mitochondrial reactive oxygen species, reduced mitochondrial membrane potential, mitochondrial calcium imbalance, mitochondrial DNA damage, and abnormal mitophagy. Accumulating evidence indicates that mitochondrial dysregulation causes oxidative stress, inflammasome activation, apoptosis, senescence, and metabolic reprogramming. All these cellular processes participate in the pathogenesis and progression of chronic respiratory diseases, including chronic obstructive pulmonary disease, pulmonary fibrosis, and asthma. In this review, we provide a comprehensive and updated overview of the impact of mitochondrial dysfunction on cellular processes involved in the development of these respiratory diseases. This not only implicates mechanisms of mitochondrial dysfunction for the pathogenesis of chronic lung diseases but also provides potential therapeutic approaches for these diseases by targeting dysfunctional mitochondria.

scholarly journals Dietary Tocotrienol/γ-Cyclodextrin Complex Increases Mitochondrial Membrane Potential and ATP Concentrations in the Brains of Aged Mice

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Anke Schloesser ◽  
Tuba Esatbeyoglu ◽  
Stefanie Piegholdt ◽  
Janina Dose ◽  
Naoko Ikuta ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Function ◽  
Mitochondrial Membrane ◽  
Heme Oxygenase 1 ◽  
Mrna Levels ◽  
Cyclodextrin Complex ◽  
Aged Mice ◽  
Atp Levels ◽  
The Brain

Brain aging is accompanied by a decrease in mitochondrial function. In vitro studies suggest that tocotrienols, includingγ- andδ-tocotrienol (T3), may exhibit neuroprotective properties. However, little is known about the effect of dietary T3 on mitochondrial function in vivo. In this study, we monitored the effect of a dietary T3/γ-cyclodextrin complex (T3CD) on mitochondrial membrane potential and ATP levels in the brain of 21-month-old mice. Mice were fed either a control diet or a diet enriched with T3CD providing 100 mg T3 per kg diet for 6 months. Dietary T3CD significantly increased mitochondrial membrane potential and ATP levels compared to those of controls. The increase in MMP and ATP due to dietary T3CD was accompanied by an increase in the protein levels of the mitochondrial transcription factor A (TFAM). Furthermore, dietary T3CD slightly increased the mRNA levels of superoxide dismutase,γ-glutamyl cysteinyl synthetase, and heme oxygenase 1 in the brain. Overall, the present data suggest that T3CD increases TFAM, mitochondrial membrane potential, and ATP synthesis in the brains of aged mice.

scholarly journals A Walnut Diet in Combination with Enriched Environment Improves Cognitive Function and Affects Lipid Metabolites in Brain and Liver of Aged NMRI Mice

2020 ◽  
Author(s):  
Carsten Esselun ◽  
Benjamin Dilberger ◽  
Carmina V. Silaidos ◽  
Elisabeth Koch ◽  
Nils Helge Schebb ◽  
...  
Keyword(s):  
Physical Activity ◽  
Synaptic Plasticity ◽  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Function ◽  
Mitochondrial Respiration ◽  
Mitochondrial Membrane ◽  
Nmri Mice ◽  
Y Maze ◽  
The Brain

AbstractThis in vivo study aimed to test if a diet enriched with 6% walnuts alone or in combination with physical activity supports healthy ageing by changing the oxylipin profile in brain and liver, improving motor function, cognition, and cerebral mitochondrial function. Female NMRI mice were fed a 6% walnut diet starting at an age of 12 months for 24 weeks. One group was additionally maintained in an enriched environment, one group without intervention served as control. After three months, one additional control group of young mice (3 weeks old) was introduced. Motor and cognitive functions were measured using Open Field, Y-Maze, Rotarod and Passive Avoidance tests. Lipid metabolite profiles were determined using RP-LC-ESI(-)-MS/MS in brain and liver tissues of mice. Cerebral mitochondrial function was characterized by the determination of ATP levels, mitochondrial membrane potential and mitochondrial respiration. Expression of genes involved with mito- and neurogenesis, inflammation, and synaptic plasticity were determined using qRT-PCR. A 6% walnut-enriched diet alone improved spatial memory in a Y-Maze alternation test (p < 0.05) in mice. Additional physical enrichment enhanced the significance, although the overall benefit was virtually identical. Instead, physical enrichment improved motor performance in a Rotarod experiment (p* < 0.05) which was unaffected by walnuts alone. Bioactive oxylipins like hydroxy-polyunsaturated fatty acids (OH-PUFA) derived from linoleic acid (LA) were significantly increased in brain (p** < 0.01) and liver (p*** < 0.0001) compared to control mice, while OH-PUFA of α-linolenic acid (ALA) could only be detected in the brains of mice fed with walnuts. In the brain, walnuts combined with physical activity reduced arachidonic acid (ARA)-based oxylipin levels (p < 0.05). Effects of walnut lipids were not linked to mitochondrial function, as ATP production, mitochondrial membrane potential and mitochondrial respiration were unaffected. Furthermore, common markers for synaptic plasticity and neuronal growth, key genes in the regulation of cytoprotective response to oxidative stress and neuronal growth were unaffected. Taken together, walnuts change the oxylipin profile in liver and brain, which could have beneficial effects for healthy ageing, an effect that can be further enhanced with an active lifestyle. Further studies may focus on specific nutrient lipids that potentially provide preventive effects in the brain.

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