scholarly journals The Relationship between Myoglobin, Aerobic Capacity, Nitric Oxide Synthase Activity and Mitochondrial Function in Fish Hearts

Antioxidants ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1072
Author(s):  
Lucie Gerber ◽  
Kathy A. Clow ◽  
William R. Driedzic ◽  
Anthony K. Gamperl
Keyword(s):  
Nitric Oxide ◽  
Mitochondrial Function ◽  
Citrate Synthase ◽  
Coupling Efficiency ◽  
Hypoxia Tolerance ◽  
Compensatory Mechanisms ◽  
Dynamic Interactions ◽  
Myoxocephalus Scorpius ◽  
Species Production ◽  
Oxide Synthase

The dynamic interactions between nitric oxide (NO) and myoglobin (Mb) in the cardiovascular system have received considerable attention. The loss of Mb, the principal O2 carrier and a NO scavenger/producer, in the heart of some red-blooded fishes provides a unique opportunity for assessing this globin’s role in NO homeostasis and mitochondrial function. We measured Mb content, activities of enzymes of NO and aerobic metabolism [NO Synthase (NOS) and citrate synthase, respectively] and mitochondrial parameters [Complex-I and -I+II respiration, coupling efficiency, reactive oxygen species production/release rates and mitochondrial sensitivity to inhibition by NO (i.e., NO IC50)] in the heart of three species of red-blooded fish. The expression of Mb correlated positively with NOS activity and NO IC50, with low NOS activity and a reduced NO IC50 in the Mb-lacking lumpfish (Cyclopterus lumpus) as compared to the Mb-expressing Atlantic salmon (Salmo salar) and short-horned sculpin (Myoxocephalus scorpius). Collectively, our data show that NO levels are fine-tuned so that NO homeostasis and mitochondrial function are preserved; indicate that compensatory mechanisms are in place to tightly regulate [NO] and mitochondrial function in a species without Mb; and strongly suggest that the NO IC50 for oxidative phosphorylation is closely related to a fish’s hypoxia tolerance.

scholarly journals Nitric Oxide Synthase-3 Overexpression Causes Apoptosis and Impairs Neuronal Mitochondrial Function: Relevance to Alzheimer's-Type Neurodegeneration

2003 ◽  
Vol 83 (2) ◽  
pp. 287-298 ◽  
Author(s):  
Suzanne M de la Monte ◽  
Jean-Daniel Chiche ◽  
Annette von dem Bussche ◽  
Sohini Sanyal ◽  
Stephanie A Lahousse ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Mitochondrial Function ◽  
Nitric Oxide Synthase 3 ◽  
Oxide Synthase

Danshensu Attenuates Hypoxia-Induced Reactive Oxygen Species Production and Inducible Nitric Oxide Synthase Expression in RAW 264.7 Cells

2019 ◽  
Vol 18 (1) ◽  
pp. 89-95
Author(s):  
Lin Chih-Hung ◽  
Lan Chou-Chin ◽  
Chiu Valeria ◽  
Hsieh Po-Chun ◽  
Kuo Chan-Yen ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Reactive Oxygen Species Production ◽  
Reactive Oxygen ◽  
Raw 264.7 Cells ◽  
Raw 264.7 ◽  
Oxygen Species ◽  
Species Production ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

Danshensu, isolated from Salvia miltiorrhiza (Danshen), is known to have anti-inflammatory properties. Therefore danshen is extensively used in many nutraceutical formulations. Reactive oxygen species are essential for the development of hypoxia-induced inflammation. Generation of reactive oxygen species by infiltrating macrophages is common in various diseases such as cardiovascular disease, neurodegenerative disease, tumor, and aging. To explore the mechanism underlying the attenuation of inflammation, we used RAW 264.7 cells as a model and hypoxia as an inducer of inflammation. The results showed the protective mechanism of danshensu on reactive oxygen species production, hypoxia-inducible factor 1-alpha expression, c-Jun N-terminal kinase phosphorylation, nuclear translocation of nuclear factor kappa B, and inducible nitric oxide synthase expression following hypoxia in RAW 264.7 cells.

Evaluation of islet heme oxygenase-CO and nitric oxide synthase-NO pathways during acute endotoxemia

2001 ◽  
Vol 280 (5) ◽  
pp. C1242-C1254 ◽  
Author(s):  
Ragnar Henningsson ◽  
Per Alm ◽  
Ingmar Lundquist
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Heme Oxygenase ◽  
Insulin Response ◽  
Glucagon Secretion ◽  
No Production ◽  
Compensatory Mechanisms ◽  
Oxide Synthase

We investigated, by a combined in vivo and in vitro approach, the temporal changes of islet nitric oxide synthase (NOS)-derived nitric oxide (NO) and heme oxygenase (HO)-derived carbon monoxide (CO) production in relation to insulin and glucagon secretion during acute endotoxemia induced by lipopolysaccharide (LPS) in mice. Basal plasma glucagon, islet cAMP and cGMP content after in vitro incubation, the insulin response to glucose in vivo and in vitro, and the insulin and glucagon responses to the adenylate cyclase activator forskolin were greatly increased after LPS. Immunoblots demonstrated expression of inducible NOS (iNOS), inducible HO (HO-1), and an increased expression of constitutive HO (HO-2) in islet tissue. Immunocytochemistry revealed a marked expression of iNOS in many β-cells, but only in single α-cells after LPS. Moreover, biochemical analysis showed a time dependent and markedly increased production of NO and CO in these islets. Addition of a NOS inhibitor to such islets evoked a marked potentiation of glucose-stimulated insulin release. Finally, after incubation in vitro, a marked suppression of NO production by both exogenous CO and glucagon was observed in control islets. This effect occurred independently of a concomitant inhibition of guanylyl cyclase. We suggest that the impairing effect of increased production of islet NO on insulin secretion during acute endotoxemia is antagonized by increased activities of the islet cAMP and HO-CO systems, constituting important compensatory mechanisms against the noxious and diabetogenic actions of NO in endocrine pancreas.

scholarly journals Mitochondrial Function in Oxidative and Glycolytic Bovine Skeletal Muscle Postmortem

2019 ◽  
Vol 3 (2) ◽  
Author(s):  
P. Ramos ◽  
L. Bell ◽  
S. Wohlgemuth ◽  
T. Scheffler
Keyword(s):  
Cytochrome C ◽  
Oxidative Phosphorylation ◽  
Outer Membrane ◽  
Functional Properties ◽  
Mitochondrial Function ◽  
Complex I ◽  
Fixed Effects ◽  
Citrate Synthase ◽  
Electron Flow ◽  
Coupling Efficiency

ObjectivesMitochondrial function in postmortem muscle is affected by decreasing oxygenation. Functional properties relating to energy production and integrity of mitochondria may influence development of meat quality characteristics. Therefore, the objective was to evaluate changes in mitochondrial function in oxidative and glycolytic muscles during the first 24h postmortem.Materials and MethodsSteers (n = 6) of primarily Angus (80 to 100%) genetics were harvested at approximately 18.5 mo and 630 kg live weight. Samples from the longissimus lumborum (LL) and diaphragm (Dia) were collected at 1, 3, and 24h postmortem. Fresh-preserved muscle samples were permeabilized using saponin, and muscle bundles (2–4 mg) were transferred to a high-resolution oxygraph for respiration measurements (oxygen consumption rate, OCR, pmol/sec/mg of tissue). Samples were assessed in duplicate under hyperoxia. First, pyruvate and malate were added to support the TCA cycle and assess leak respiration. Then, ADP was added to support electron flow through complex I. The influence of glutamate on NADH production (complex I) was tested, followed by complex II activation by succinate. Integrity of the mitochondria outer membrane was tested with cytochrome c. Next, an uncoupler (FCCP) was added to force the electron transport system (ETS) to maximum capacity. Citrate synthase (CS) activity (nmol/min/mg tissue) was determined in frozen samples and used as a marker of mitochondria content. Subsequently, respiration data were normalized to CS activity (pmol/sec/U CS) to account for differences in mitochondria content. Coupling efficiency of oxidative phosphorylation was calculated as 1– (Leak/ADP-stimulated oxidative phosphorylation capacity). Raw and normalized OCR were analyzed in a randomized block design, with slaughter date as block and fixed effects of muscle, time, and the interaction. Time was considered a repeated measure.ResultsMuscle type affected (P = 0.0002) leak OCR, with Dia showing a higher rate than LL. After ADP was added, mitochondria from Dia exhibited higher OCR at all times tested and at all steps, with OCR being 4 times higher after FCCP addition. Mitochondrial content, evidenced by greater (P < 0.0001) CS activity in Dia, largely explained differences in OCR between muscles. After OCR was normalized to CS activity, the 1 and 3h postmortem OCR from Dia and LL were similar (P > 0.05). However, at 24h postmortem, OCR after ADP, glutamate, and FCCP additions were greater (P < 0.05) in Dia mitochondria. Time, but not muscle, affected cytochrome c response. At 1h postmortem, cytochrome c increased OCR by 6.6%, supporting that mitochondria outer membrane integrity is not compromised. However, cytochrome c response at 3h postmortem increased 52.4%, indicating outer membrane damage. Coupling efficiency is different between muscles (P = 0.005) with Dia exhibiting greater efficiency.ConclusionDespite inherent metabolic differences between the LL and Dia, mitochondria from both muscles are intact and coupled at 1h postmortem. However, by 24h postmortem, functional properties of LL mitochondria are reduced compared to Dia. Declining mitochondrial function may be associated with calcium overload, mitochondrial fragmentation, and protease activation.

scholarly journals Powerhouses in the cold: mitochondrial function during thermal acclimation in montane mayflies

2019 ◽  
Vol 375 (1790) ◽  
pp. 20190181 ◽  
Author(s):  
Justin C. Havird ◽  
Alisha A. Shah ◽  
Adam J. Chicco
Keyword(s):  
Mitochondrial Function ◽  
Citrate Synthase ◽  
Coupling Efficiency ◽  
High Elevation ◽  
Thermal Acclimation ◽  
Environmental Adaptation ◽  
Genetic Changes ◽  
Mitochondrial Genotype ◽  
Complex Relationships ◽  
Titration Protocol

Mitochondria provide the vast majority of cellular energy available to eukaryotes. Therefore, adjustments in mitochondrial function through genetic changes in mitochondrial or nuclear-encoded genes might underlie environmental adaptation. Environmentally induced plasticity in mitochondrial function is also common, especially in response to thermal acclimation in aquatic systems. Here, we examined mitochondrial function in mayfly larvae ( Baetis and Drunella spp.) from high and low elevation mountain streams during thermal acclimation to ecologically relevant temperatures. A multi-substrate titration protocol was used to evaluate different respiratory states in isolated mitochondria, along with cytochrome oxidase and citrate synthase activities. In general, maximal mitochondrial respiratory capacity and oxidative phosphorylation coupling efficiency decreased during acclimation to higher temperatures, suggesting montane insects may be especially vulnerable to rapid climate change. Consistent with predictions of the climate variability hypothesis, mitochondria from Baetis collected at a low elevation site with highly variable daily and seasonal temperatures exhibited greater thermal tolerance than Baetis from a high elevation site with comparatively stable temperatures. However, mitochondrial phenotypes were more resilient than whole-organism phenotypes in the face of thermal stress. These results highlight the complex relationships between mitochondrial and organismal genotypes, phenotypes and environmental adaptation. This article is part of the theme issue ‘Linking the mitochondrial genotype to phenotype: a complex endeavour’.

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