scholarly journals Cardiac mitochondrial plasticity and thermal sensitivity in a fish inhabiting an artificially heated ecosystem

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Nicolas Pichaud ◽  
Andreas Ekström ◽  
Sophie Breton ◽  
Fredrik Sundström ◽  
Piotr Rowinski ◽  
...  
Keyword(s):  
Citrate Synthase ◽  
Thermal Sensitivity ◽  
Natural Habitat ◽  
Perca Fluviatilis ◽  
Adjacent Area ◽  
Adaptive Responses ◽  
Mitochondrial Functions ◽  
The Baltic ◽  
Laboratory Acclimation ◽  
Environmental Warming

AbstractSome evidence suggests that cardiac mitochondrial functions might be involved in the resilience of ectotherms such as fish to environmental warming. Here, we investigated the effects of acute and chronic changes in thermal regimes on cardiac mitochondrial plasticity and thermal sensitivity in perch (Perca fluviatilis) from an artificially heated ecosystem; the “Biotest enclosure” (~25 °C), and from an adjacent area in the Baltic Sea with normal temperatures (reference, ~16 °C). We evaluated cardiac mitochondrial respiration at assay temperatures of 16 and 25 °C, as well as activities of lactate dehydrogenase (LDH) and citrate synthase (CS) in Biotest and reference perch following 8 months laboratory-acclimation to either 16 or 25 °C. While both populations exhibited higher acute mitochondrial thermal sensitivity when acclimated to their natural habitat temperatures, this sensitivity was lost when Biotest and reference fish were acclimated to 16 and 25 °C, respectively. Moreover, reference fish displayed patterns of metabolic thermal compensation when acclimated to 25 °C, whereas no changes were observed in Biotest perch acclimated to 16 °C, suggesting that cardiac mitochondrial metabolism of Biotest fish expresses local adaptation. This study highlights the adaptive responses of cardiac mitochondria to environmental warming, which can impact on fish survival and distribution in a warming climate.

Schisandrin Restores the Amyloid β-Induced Impairments on Mitochondrial Function, Energy Metabolism, Biogenesis, and Dynamics in Rat Primary Hippocampal Neurons

Pharmacology ◽  
2021 ◽  
pp. 1-11
Author(s):  
Zhongyuan Piao ◽  
Lin Song ◽  
Lifen Yao ◽  
Limei Zhang ◽  
Yichan Lu
Keyword(s):  
Energy Metabolism ◽  
Cytochrome C ◽  
Mitochondrial Biogenesis ◽  
Mitochondrial Function ◽  
Hippocampal Neurons ◽  
Citrate Synthase ◽  
Mitochondrial Permeability Transition ◽  
Amyloid Β ◽  
Mitochondrial Functions ◽  
Primary Hippocampal Neurons

Introduction: Schisandrin which is derived from Schisandra chinensis has shown multiple pharmacological effects on various diseases including Alzheimer’s disease (AD). It is demonstrated that mitochondrial dysfunction plays an essential role in the pathogenesis of neurodegenerative disorders. Objective: Our study aims to investigate the effects of schisandrin on mitochondrial functions and metabolisms in primary hippocampal neurons. Methods: In our study, rat primary hippocampal neurons were isolated and treated with indicated dose of amyloid β1–42 (Aβ1–42) oligomer to establish a cell model of AD in vitro. Schisandrin (2 μg/mL) was further subjected to test its effects on mitochondrial function, energy metabolism, mitochondrial biogenesis, and dynamics in the Aβ1–42 oligomer-treated neurons. Results and Conclusions: Our findings indicated that schisandrin significantly alleviated the Aβ1–42 oligomer-induced loss of mitochondrial membrane potential and impaired cytochrome c oxidase activity. Additionally, the opening of mitochondrial permeability transition pore and release of cytochrome c were highly restricted with schisandrin treatment. Alterations in cell viability, ATP production, citrate synthase activity, and the expressions of glycolysis-related enzymes demonstrated the relief of defective energy metabolism in Aβ-treated neurons after the treatment of schisandrin. For mitochondrial biogenesis, elevated expression of peroxisome proliferator-activated receptor γ coactivator along with promoted mitochondrial mass was found in schisandrin-treated cells. The imbalance in the cycle of fusion and fission was also remarkably restored by schisandrin. In summary, this study provides novel mechanisms for the protective effect of schisandrin on mitochondria-related functions.

scholarly journals DNA methyltransferase 3a mediates developmental thermal plasticity

BMC Biology ◽  
2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Isabella Loughland ◽  
Alexander Little ◽  
Frank Seebacher
Keyword(s):  
Environmental Change ◽  
Dna Methyltransferase ◽  
Developmental Plasticity ◽  
Citrate Synthase ◽  
Thermal Sensitivity ◽  
Short Term ◽  
Cold Temperatures ◽  
Knock Out ◽  
Thermal Plasticity ◽  
Dna Methyltransferase 3A

Abstract Background Thermal plasticity is pivotal for evolution in changing climates and in mediating resilience to its potentially negative effects. The efficacy to respond to environmental change depends on underlying mechanisms. DNA methylation induced by DNA methyltransferase 3 enzymes in the germline or during early embryonic development may be correlated with responses to environmental change. This developmental plasticity can interact with reversible acclimation within adult organisms, which would increase the speed of response and could alleviate potential mismatches between parental or early embryonic environments and those experienced at later life stages. Our aim was to determine whether there is a causative relationship between DNMT3 enzyme and developmental thermal plasticity and whether either or both interact with short-term acclimation to alter fitness and thermal responses in zebrafish (Danio rerio). Results We developed a novel DNMT3a knock-out model to show that sequential knock-out of DNA methyltransferase 3a isoforms (DNMT3aa−/− and DNMT3aa−/−ab−/−) additively decreased survival and increased deformities when cold developmental temperatures in zebrafish offspring mismatched warm temperatures experienced by parents. Interestingly, short-term cold acclimation of parents before breeding rescued DNMT3a knock-out offspring by restoring survival at cold temperatures. DNMT3a knock-out genotype interacted with developmental temperatures to modify thermal performance curves in offspring, where at least one DNMT3a isoform was necessary to buffer locomotion from increasing temperatures. The thermal sensitivity of citrate synthase activity, an indicator of mitochondrial density, was less severely affected by DNMT3a knock-out, but there was nonetheless a significant interaction between genotype and developmental temperatures. Conclusions Our results show that DNMT3a regulates developmental thermal plasticity and that the phenotypic effects of different DNMT3a isoforms are additive. However, DNMT3a interacts with other mechanisms, such as histone (de)acetylation, induced during short-term acclimation to buffer phenotypes from environmental change. Interactions between these mechanisms make phenotypic compensation for climate change more efficient and make it less likely that thermal plasticity incurs a cost resulting from environmental mismatches.

scholarly journals Adult female European perch (Perca fluviatilis) from the Baltic Sea show no evidence of thiamine deficiency

2021 ◽  
pp. 102081
Author(s):  
Johan Gustafsson ◽  
Karin Ström ◽  
Linus Arvstrand ◽  
Lars Förlin ◽  
Lillemor Asplund ◽  
...  
Keyword(s):  
Baltic Sea ◽  
Adult Female ◽  
Thiamine Deficiency ◽  
Perca Fluviatilis ◽  
The Baltic Sea ◽  
European Perch ◽  
Perch Perca Fluviatilis ◽  
The Baltic

Impaired Mitochondrial functions and Energy Metabolism in MPTP-induced Model of Parkinson’s Disease in Mice: Comparison of Strains and Dose Regimens

2021 ◽  
Author(s):  
Anjana Pathania ◽  
Priyanka Garg ◽  
Rajat Sandhir
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Membrane Potential ◽  
Metabolic Pathways ◽  
Citrate Synthase ◽  
Mitochondrial Respiratory Chain ◽  
Progression Rate ◽  
Mitochondrial Dysfunctions ◽  
Mitochondrial Functions ◽  
Mptp Treatment

Abstract Parkinson’s disease is a multiplexed disease involving diverse symptoms and progression rate. Heterogenous diseases need an efficient animal model to enhance the understanding of the underlying mechanism. MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine), a neurotoxin, has been widely used to replicate the pathophysiology of PD in rodents, but its effect on energy metabolic perturbation is limited. Moreover, susceptibility to different dosage regime of MPTP varies among mice strains. Thus, herein the present study compares the effect of acute and sub-acute MPTP dosage regimes on mitochondrial functions in terms of mitochondrial respiratory chain enzymes, mitochondrial swelling and membrane potential in C57BL/6 and Balb/c mice. In addition, activities of enzymes involved in energy metabolic pathways were also studied along with behaviour and neurochemical alterations. The results showed that acute dose of MPTP in C57BL/6 mice had more profound effect on the enzyme activities of electron transport chain complexes. Further, the activity of MAO-A and MAO-B was increased following acute and sub-acute MPTP administration in C57BL/6 mice. However, no significant change was observed in Balb/c strain. Acute MPTP treatment resulted in decreased mitochondrial membrane potential along with swelling of mitochondria in C57BL/6 mice. In addition, perturbations were observed in hexokinase and pyruvate dehydrogenase of glycolysis pathway and citrate synthase, aconitase, isocitrate dehydrogenase and fumarase of TCA cycle. Moreover, acute MPTP led to pronounced depletion in neostriatal dopamine levels in C57BL/6 than in Balb/c mice. Behavioral tests such as open field, Narrow beam walk test and footprint test showed that locomotor activity was drastically reduced as an acute effect of MPTP in C57BL/6 mice strain. Therefore, these results consistently showed that acute MPTP treatment in C57BL/6 strain had severe mitochondrial dysfunctions, perturbed energy metabolic pathways, altered neurotransmission and motor defects as compared to Balb/c strain. Thus, the findings suggest that the dose and strain of mice need to consider for pre-clinical studies targeting mitochondrial dysfunctions in MPTP-induced Parkinson’s disease model.

scholarly journals Does a cannibal feeding strategy impart differential metabolic performance in young burbot (Lota lota maculosa)?

2020 ◽  
Vol 8 (1) ◽  
Author(s):  
Amanda J Frazier ◽  
Nathan R Jensen ◽  
Shawn P Young ◽  
Anne E Todgham
Keyword(s):  
Citrate Synthase ◽  
Feeding Strategy ◽  
Natural Habitat ◽  
Resting Metabolic Rate ◽  
Habitat Alteration ◽  
Traditional Practice ◽  
Wild Stock ◽  
Lota Lota ◽  
Leading Role ◽  
Metabolic Performance

Abstract The practice of mitigating cannibalism in aquaculture is an important focus for hatcheries seeking to maximize yield and has been maintained in hatcheries focusing on wild stock restoration. We hypothesize, however, that a cannibal feeding strategy may confer performance advantages over a non-cannibal feeding strategy and that perhaps cannibal size grading may not be optimal for hatcheries focusing on conservation goals. This study examined metabolic performance differences between cannibal and non-cannibal burbot, Lota lota maculosa, at the Kootenai Tribe of Idaho Twin Rivers Hatchery in Moyie Springs, ID, USA. After habitat alteration led to functional extinction of burbot in the region, the Twin Rivers Hatchery has played a leading role in the reestablishment of burbot in the Kootenai River, ID, and British Columbia. We examined morphometric data (weight, length and condition factor), whole animal resting metabolic rate and the enzyme activity of lactate dehydrogenase, citrate synthase and 3-hydroxyacyl-CoA dehydrogenase to describe the baseline metabolic performance of cannibal and non-cannibal burbot. Taken together, our results demonstrated significant differences in the metabolic strategies of cannibal vs. non-cannibal burbot, where cannibals relied more heavily on carbohydrate metabolism and non-cannibals relied more heavily on glycolytic and lipid metabolism. This study demonstrates the need to reevaluate the traditional practice of removing cannibal fish in conservation hatcheries, as it may not be the ideal strategy of raising the most robust individuals for release. When natural habitat conditions cannot be restored due to permanent habitat alteration, prioritizing release of higher performing individuals could help achieve conservation goals.

scholarly journals The biophysical basis of thermal tolerance in fish eggs

2020 ◽  
Vol 287 (1937) ◽  
pp. 20201550
Author(s):  
Benjamin T. Martin ◽  
Peter N. Dudley ◽  
Neosha S. Kashef ◽  
David M. Stafford ◽  
William J. Reeder ◽  
...  
Keyword(s):  
Chinook Salmon ◽  
Thermal Tolerance ◽  
Oncorhynchus Tshawytscha ◽  
Fundamental Problem ◽  
Thermal Sensitivity ◽  
Supply And Demand ◽  
Natural Habitat ◽  
Mechanistic Explanation ◽  
Biophysical Model ◽  
Warming Climate

A warming climate poses a fundamental problem for embryos that develop within eggs because their demand for oxygen (O 2 ) increases much more rapidly with temperature than their capacity for supply, which is constrained by diffusion across the egg surface. Thus, as temperatures rise, eggs may experience O 2 limitation due to an imbalance between O 2 supply and demand. Here, we formulate a mathematical model of O 2 limitation and experimentally test whether this mechanism underlies the upper thermal tolerance in large aquatic eggs. Using Chinook salmon ( Oncorhynchus tshawytscha ) as a model system, we show that the thermal tolerance of eggs varies systematically with features of the organism and environment. Importantly, this variation can be precisely predicted by the degree to which these features shift the balance between O 2 supply and demand. Equipped with this mechanistic understanding, we predict and experimentally confirm that the thermal tolerance of these embryos in their natural habitat is substantially lower than expected from laboratory experiments performed under normoxia. More broadly, our biophysical model of O 2 limitation provides a mechanistic explanation for the elevated thermal sensitivity of fish embryos relative to other life stages, global patterns in egg size and the extreme fecundity of large teleosts.

Thermal acclimation in Antarctic fish: transcriptomic profiling of metabolic pathways

2011 ◽  
Vol 301 (5) ◽  
pp. R1453-R1466 ◽  
Author(s):  
Heidrun Sigrid Windisch ◽  
Raphaela Kathöver ◽  
Hans-Otto Pörtner ◽  
Stephan Frickenhaus ◽  
Magnus Lucassen
Keyword(s):  
Phosphoenolpyruvate Carboxykinase ◽  
Citrate Synthase ◽  
Thermal Sensitivity ◽  
Antarctic Fish ◽  
Control Group ◽  
Acclimation Temperature ◽  
Peroxisome Proliferator ◽  
Warm Acclimation ◽  
Peroxisome Proliferator Activated Receptors ◽  
Large Rearrangements

It is widely accepted that adaptation to the extreme cold has evolved at the expense of high thermal sensitivity. However, recent studies have demonstrated significant capacities for warm acclimation in Antarctic fishes. Here, we report on hepatic metabolic reorganization and its putative molecular background in the Antarctic eelpout ( Pachycara brachycephalum ) during warm acclimation to 5°C over 6 wk. Elevated capacities of cytochrome c oxidase suggest the use of warm acclimation pathways different from those in temperate fish. The capacity of this enzyme rose by 90%, while citrate synthase (CS) activity fell by 20% from the very beginning. The capacity of lipid oxidation by hydroxyacyl-CoA dehydrogenase remained constant, whereas phosphoenolpyruvate carboxykinase as a marker for gluconeogenesis displayed 40% higher activities. These capacities in relation to CS indicate a metabolic shift from lipid to carbohydrate metabolism. The finding was supported by large rearrangements of the related transcriptome, both functional genes and potential transcription factors. A multivariate analysis (canonical correspondence analyses) of various transcripts subdivided the incubated animals in three groups, one control group and two responding on short and long timescales, respectively. A strong dichotomy in the expression of peroxisome proliferator-activated receptors-1α and -β receptors was most striking and has not previously been reported. Altogether, we identified a molecular network, which responds sensitively to warming beyond the realized ecological niche. The shift from lipid to carbohydrate stores and usage may support warm hardiness, as the latter sustain anaerobic metabolism and may prepare for hypoxemic conditions that would develop upon warming beyond the present acclimation temperature.

scholarly journals Effects of peroxisome proliferator activated receptor gamma (PPARɣ) agonist on fasting model applied neuron cultures

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Arzu Pınarbaşı ◽  
Meltem Pak ◽  
Murat Kolay ◽  
Devrim Öz Arslan ◽  
Fehime Benli Aksungar
Keyword(s):  
Neurodegenerative Diseases ◽  
Citrate Synthase ◽  
Neuronal Cells ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Lactate Dehydrogenase Activity ◽  
Energy Metabolites ◽  
Pparγ Agonist ◽  
Mitochondrial Functions ◽  
Pparγ Agonists

Abstract Objectives Peroxisome proliferator activated receptor gamma (PPARγ) agonists used for the treatment of Diabetes Mellitus (DM), has important roles on the regulation of metabolism including ketogenesis in fasting and low glucose states. Recently PPARγ was proven to have anti-oxidant and anti-inflammatory effects on neuronal cells. Methods In the present study, effects of pioglitazone (PPARγ agonist) on cell survival, energy metabolism and mitochondrial functions were investigated in glucose deprived fasting model applied SH-SY5Y (ATCC/CRL 2266) cell lines. Before and after pioglitazone treatment; energy metabolites (glucose, lactate, ketone (βOHB), lactate dehydrogenase activity), mitochondrial citrate synthase activity and cell viability were investigated. Results and Conclusions PPARγ agonist addition to glucose deprived, ketone added neurons provided positive improvements in energy metabolites (p<0.01), mitochondrial functions (p<0.001) and survival rates (p<0.01). Changes in mitochondrial citrate synthase activity, lactate and LDH levels of neuronal cells treated with PPARγ agonist have not been previously shown. Our results suggest, pioglitazone as an effective alternative for the treatment of neurodegenerative diseases especially with the presence of ketone bodies. By clarifying the mechanisms of PPARγ agonists, a great contribution will be made to the treatment of neurodegenerative diseases.

scholarly journals Cardiorespiratory adjustments to chronic environmental warming improve hypoxia tolerance in European perch (Perca fluviatilis)

2021 ◽  
pp. jeb.241554
Author(s):  
Andreas Ekström ◽  
Erika Sundell ◽  
Daniel Morgenroth ◽  
Tristan McArley ◽  
Anna Gårdmark ◽  
...  
Keyword(s):  
Climate Warming ◽  
Nuclear Power ◽  
Acute Hypoxia ◽  
Cooling Water ◽  
Perca Fluviatilis ◽  
Thermal Acclimation ◽  
Hypoxia Tolerance ◽  
Physiological Traits ◽  
European Perch ◽  
Environmental Warming

Aquatic hypoxia will become increasingly prevalent in the future due to eutrophication combined with climate warming. While short-term warming typically constrains fish hypoxia tolerance, many fishes cope with warming by adjusting physiological traits through thermal acclimation. Yet, little is known about how such adjustments affect tolerance to hypoxia.We examined European perch (Perca fluviatilis) from the Biotest enclosure (23°C, Biotest population), a unique ∼1 km2 ecosystem artificially warmed by cooling water from a nuclear power plant, and an adjacent reference site (16-18°C, Reference population). Specifically, we evaluated how acute and chronic warming affect routine oxygen consumption rate (MO2routine) and cardiovascular performance in acute hypoxia, alongside assessments of the thermal acclimation of the aerobic contribution to hypoxia tolerance (critical O2 tension for MO2routine; Pcrit) and absolute hypoxia tolerance (O2 tension at loss of equilibrium; PLOE).Chronic adjustments (possibly across lifetime or generations) alleviated energetic costs of warming in Biotest perch by depressing MO2routine and cardiac output, and by increasing blood O2 carrying capacity relative to reference perch acutely warmed to 23°C. These adjustments were associated with improved maintenance of cardiovascular function and MO2routine in hypoxia (i.e., reduced Pcrit). However, while Pcrit was only partially thermally compensated in Biotest perch, they had superior absolute hypoxia tolerance (i.e., lowest PLOE) relative to reference perch irrespective of temperature.We show that European perch can thermally adjust physiological traits to safeguard and even improve hypoxia tolerance during chronic environmental warming. This points to cautious optimism that eurythermal fish species may be resilient to the imposition of impaired hypoxia tolerance with climate warming.

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