Mitochondrial function in flying honeybees (Apis mellifera): respiratory chain enzymes and electron flow from complex III to oxygen

The biochemical bases for the high mass-specific metabolic rates of flying insects remain poorly understood. To gain insights into mitochondrial function during flight, metabolic rates of individual flying honeybees were measured using respirometry, and their thoracic muscles were fixed for electron microscopy. Mitochondrial volume densities and cristae surface densities, combined with biochemical data concerning cytochrome content per unit mass, were used to estimate respiratory chain enzyme densities per unit cristae surface area. Despite the high content of respiratory enzymes per unit muscle mass, these are accommodated by abundant mitochondria and high cristae surface densities such that enzyme densities per unit cristae surface area are similar to those found in mammalian muscle and liver. These results support the idea that a unit area of mitochondrial inner membrane constitutes an invariant structural unit. Rates of O(2) consumption per unit cristae surface area are much higher than those estimated in mammals as a consequence of higher enzyme turnover rates (electron transfer rates per enzyme molecule) during flight. Cytochrome c oxidase, in particular, operates close to its maximum catalytic capacity (k(cat)). Thus, high flux rates are achieved via (i) high respiratory enzyme content per unit muscle mass and (ii) the operation of these enzymes at high fractional velocities.

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Trib1 deficiency causes brown adipose respiratory chain depletion and mitochondrial disorder

Cell Death and Disease ◽

10.1038/s41419-021-04389-x ◽

2021 ◽

Vol 12 (12) ◽

Author(s):

Xuelian Zhang ◽

Bin Zhang ◽

Chenyang Zhang ◽

Guibo Sun ◽

Xiaobo Sun

Keyword(s):

Adipose Tissue ◽

Respiratory Chain ◽

Mitochondrial Function ◽

Knockout Mice ◽

Mitochondrial Respiratory Chain ◽

Complex Iii ◽

Adrenoceptor Agonist ◽

Brown Adipose ◽

Mitochondrial Respiratory

AbstractTribbles homolog 1 (TRIB1) belongs to the Tribbles family of pseudokinases, which plays a key role in tumorigenesis and inflammation. Although genome-wide analysis shows that TRIB1 expression is highly correlated with blood lipid levels, the relationship between TRIB1 and adipose tissue metabolism remains unclear. Accordingly, the aim of the present study was to explore the role of TRIB1 on mitochondrial function in the brown adipose tissue (BAT). Trib1-knockout mice were established using clustered regularly interspaced short palindromic repeats (CRISPR)/Cas9 technology. The metabolic function of the BAT was induced by a β3-adrenoceptor agonist and the energy metabolism function of mitochondria in the BAT of mice was evaluated. Trib1-knockout mice exhibited obesity and impaired BAT thermogenesis. In particular, Trib1 knockout reduced the ability of the BAT to maintain body temperature, inhibited β3-adrenoceptor agonist-induced thermogenesis, and accelerated lipid accumulation in the liver and adipose tissues. In addition, Trib1 knockout reduced mitochondrial respiratory chain complex III activity, produced an imbalance between mitochondrial fusion and fission, caused mitochondrial structural damage and dysfunction, and affected heat production and lipid metabolism in the BAT. Conversely, overexpression of Trib1 in 3T3-L1 adipocytes increased the number of mitochondria and improved respiratory function. These findings support the role of Trib1 in regulating the mitochondrial respiratory chain and mitochondrial dynamics by affecting mitochondrial function and thermogenesis in the BAT.

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The nature of the stimulation of the respiratory chain of rat liver mitochondria by glucagon pretreatment of animals

Biochemical Journal ◽

10.1042/bj2040037 ◽

1982 ◽

Vol 204 (1) ◽

pp. 37-47 ◽

Cited By ~ 41

Author(s):

A P Halestrap

Keyword(s):

Respiratory Chain ◽

Electron Flow ◽

Liver Mitochondria ◽

Complex Iii ◽

Secondary Site ◽

Rat Liver Mitochondria ◽

Succinate Oxidation ◽

Q Cycle ◽

Cytochromes C ◽

Stimulation Of

1. Studies on the cytochrome spectra of liver mitochondria from control and glucagon-treated rats in State 4, State 3 and in the presence of uncoupler are reported. 2. The stimulation of electron flow between cytochromes c1 and c observed previously [Halestrap (1978) Biochem. J. 172, 399-405] was shown to be an artefact of Ca2+-induced swelling of mitochondria. 3. When precautions were taken to prevent such swelling, glucagon treatment was shown to enhance the reduction of cytochromes c, c1 and b558 in both State 3 and uncoupled conditions with either succinate or glutamate + malate as substrate. An increase in the reduction of cytochromes b562 and b566 was also seen in some, but not all, experiments. 4. In State 4 with succinate but not glutamate + malate as substrate, cytochromes c, c1, b558, b562 and b566 showed increased reduction. 5. Glucagon stimulated oxidation of duroquinol and palmitoylcarnitine by intact mitochondria and of NADH by disrupted mitochondria. 6. No effect of glucagon on succinate dehydrogenase activity or the temperature-dependence of succinate oxidation could be detected. 7. Glucagon enhanced the inhibition of the respiratory chain by colletotrichin, but not antimycin or 8-heptyl-4-hydroxyquinoline N-oxide. 8. These results are interpreted in terms of a primary stimulation by glucagon of the ‘Q cycle’ [Mitchell (1976) J. Theor. Biol. 62, 827-367] within Complex III (ubiquinol:cytochrome c oxidoreductase) and a secondary site of action involving stimulation of electron flow into Complex III from the ubiquinone pool. 9. Ageing of mitochondria, hyperosmotic treatment or addition of 20 mM-benzyl alcohol opposed the effects of glucagon treatment on cytochrome spectra and colletotrichin inhibition of respiration. 10. These results support the hypothesis that glucagon exerts its effects on the mitochondria by perturbing the membrane structure.

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The Mitochondrial Respiratory Chain Maintains the Photosynthetic Electron Flow in Arabidopsis thaliana Leaves under High-Light Stress

Plant and Cell Physiology ◽

10.1093/pcp/pcz193 ◽

2019 ◽

Vol 61 (2) ◽

pp. 283-295 ◽

Cited By ~ 2

Author(s):

Shoya Yamada ◽

Hiroshi Ozaki ◽

Ko Noguchi

Keyword(s):

Arabidopsis Thaliana ◽

Electron Transport ◽

Respiratory Chain ◽

Rate Constants ◽

Electron Flow ◽

Light Stress ◽

Photosynthetic Electron Transport ◽

Mitochondrial Respiratory Chain ◽

High Light ◽

Complex Iii

Abstract The plant respiratory chain includes the ATP-coupling cytochrome pathway (CP) and ATP-uncoupling alternative oxidase (AOX). Under high-light (HL) conditions, plants experience photoinhibition, leading to a damaged photosystem II (PSII). The respiratory chain is considered to affect PSII maintenance and photosynthetic electron transport under HL conditions. However, the underlying details remain unclear. In this study, we investigated the respiratory chain functions related to PSII maintenance and photosynthetic electron transport in plants exposed to HL stress. We measured the HL-induced decrease in the maximum quantum yield of PSII in the leaves of wild-type and AOX1a-knockout (aox1a) Arabidopsis thaliana plants in which CP was partially inhibited by a complex-III inhibitor. We also calculated PSII photodamage and repair rate constants. Both rate constants changed when CP was partially inhibited in aox1a plants, suggesting that the respiratory chain is related to both processes. Before HL stress, photosynthetic linear electron flow (LEF) decreased when CP was partially inhibited. After HL stress, aox1a in the presence of the CP inhibitor showed significantly decreased rates of LEF. The electron flow downstream from PSII and on the donor side of photosystem I may have been suppressed. The function of respiratory chain is required to maintain the optimal LEF as well as PSII maintenance especially under the HL stress.

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NIR-responsive MXene nanobelts for wound healing

NPG Asia Materials ◽

10.1038/s41427-021-00289-w ◽

2021 ◽

Vol 13 (1) ◽

Author(s):

Lin Jin ◽

Xiaoqing Guo ◽

Di Gao ◽

Cui Wu ◽

Bin Hu ◽

...

Keyword(s):

Wound Healing ◽

Vitamin E ◽

Surface Area ◽

Near Infrared ◽

Coating Layer ◽

High Surface ◽

High Surface Area ◽

High Mass ◽

Polymeric Coating ◽

Mass Loading

AbstractEffectively achieving wound healing is a great challenge. Herein, we facilely prepared temperature-responsive MXene nanobelt fibers (T-RMFs) carrying vitamin E with a controllable release ability for wound healing. These T-RMFs were composed of MXene nanosheets spread along polyacrylonitrile and polyvinylpyrrolidone composite nanobelts together with a thermosensitive PAAV- coating layer. The high mass loading and high surface area of the MXene nanosheets endow the T-RMFs with excellent photothermal properties. The temperature could be easily controlled by near-infrared (NIR) irradiation exposure, and then the thermoresponsive polymeric coating layer relaxed the interface to dissolve vitamin E and promote vitamin E release. The T-RMFs demonstrated excellent biocompatibility and wound-healing functions in cellular and animal tests. The facile method, high mass loading, high surface area, excellent wound-healing functions, interesting nanosheet/nanobelt structure, mass production potential, and NIR responsive properties of these T-RMFs indicate the great potential of our nanobelts for wound healing, tissue engineering, and much broader application areas. This facile nanosheet/nanobelt preparation strategy paves a new way for nanomaterial fabrication and applications.

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Relationships Between Propulsion and Anthropometry in Paralympic Swimmers

International Journal of Sports Physiology and Performance ◽

10.1123/ijspp.2014-0186 ◽

2015 ◽

Vol 10 (8) ◽

pp. 978-985 ◽

Cited By ~ 5

Author(s):

Andrew A. Dingley ◽

David B. Pyne ◽

Brendan Burkett

Keyword(s):

Surface Area ◽

Muscle Mass ◽

Physical Disability ◽

Swimming Performance ◽

Upper Body ◽

Swimming Velocity ◽

Frontal Surface ◽

Anthropometric Measures ◽

Arm Span ◽

Upper Body Power

Purpose:To characterize relationships between propulsion, anthropometry, and performance in Paralympic swimming.Methods:A cross-sectional study of swimmers (13 male, 15 female) age 20.5 ± 4.4 y was conducted. Subject locomotor categorizations were no physical disability (n = 8, classes S13–S14) and low-severity (n = 11, classes S9–S10) or midseverity disability (n = 9, classes S6–S8). Full anthropometric profiles estimated muscle mass and body fat, a bilateral swim-bench ergometer quantified upper-body power production, and 100-m time trials quantified swimming performance.Results:Correlations between ergometer mean power and swimming performance increased with degree of physical disability (low-severity male r = .65, ±0.56, and female r = .68, ±0.64; midseverity, r = .87, ±0.41, and r = .79, ±0.75). The female midseverity group showed nearperfect (positive) relationships for taller swimmers’ (with a greater muscle mass and longer arm span) swimming faster, while for female no- and low-severity-disability groups, greater muscle mass was associated with slower velocity (r = .78, ±0.43, and r = .65, ±0.66). This was supported with lighter females (with less frontal surface area) in the low-severity group being faster (r = .94, ±0.24). In a gender contrast, low-severity males with less muscle mass (r = -.64, ±0.56), high skinfolds (r = .78, ±0.43), a longer arm span (r = .58, ±0.60) or smaller frontal surface area (r = -.93, ±0.19) were detrimental to swimming-velocity production.Conclusion:Low-severity male and midseverity female Paralympic swimmers should be encouraged to develop muscle mass and upper-body power to enhance swimming performance. The generalized anthropometric measures appear to be a secondary consideration for coaches.

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The Effect of Voluntary Wheel Running on Muscle Mass, Mitochondrial Function and Oxidative Damage in Sod1???/???mice

Medicine & Science in Sports & Exercise ◽

10.1249/00005768-200611001-00045 ◽

2006 ◽

Vol 38 (Suppl 1) ◽

pp. S12

Author(s):

Michael S. Lustgarten ◽

Young C. Jang ◽

Wook Song ◽

Yuhong Liu ◽

Anson Pierce ◽

...

Keyword(s):

Oxidative Damage ◽

Muscle Mass ◽

Mitochondrial Function ◽

Wheel Running ◽

Voluntary Wheel Running ◽

Voluntary Wheel

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NAD + repletion produces no therapeutic effect in mice with respiratory chain complex III deficiency and chronic energy deprivation

The FASEB Journal ◽

10.1096/fj.201800090r ◽

2018 ◽

Vol 32 (11) ◽

pp. 5913-5926 ◽

Cited By ~ 9

Author(s):

Janne Purhonen ◽

Jayasimman Rajendran ◽

Saara Tegelberg ◽

Olli-Pekka Smolander ◽

Eija Pirinen ◽

...

Keyword(s):

Therapeutic Effect ◽

Respiratory Chain ◽

Chain Complex ◽

Complex Iii ◽

Respiratory Chain Complex ◽

Energy Deprivation

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Specific requirements of nonbilayer phospholipids in mitochondrial respiratory chain function and formation

Molecular Biology of the Cell ◽

10.1091/mbc.e15-12-0865 ◽

2016 ◽

Vol 27 (14) ◽

pp. 2161-2171 ◽

Cited By ~ 31

Author(s):

Charli D. Baker ◽

Writoban Basu Ball ◽

Erin N. Pryce ◽

Vishal M. Gohil

Keyword(s):

Respiratory Chain ◽

Mitochondrial Membrane ◽

Phospholipid Composition ◽

Mitochondrial Respiratory Chain ◽

Complex Iii ◽

Specific Requirement ◽

Transport Pathway ◽

Contact Sites ◽

Yeast Mutants ◽

Mitochondrial Respiratory

Mitochondrial membrane phospholipid composition affects mitochondrial function by influencing the assembly of the mitochondrial respiratory chain (MRC) complexes into supercomplexes. For example, the loss of cardiolipin (CL), a signature non–bilayer-forming phospholipid of mitochondria, results in disruption of MRC supercomplexes. However, the functions of the most abundant mitochondrial phospholipids, bilayer-forming phosphatidylcholine (PC) and non–bilayer-forming phosphatidylethanolamine (PE), are not clearly defined. Using yeast mutants of PE and PC biosynthetic pathways, we show a specific requirement for mitochondrial PE in MRC complex III and IV activities but not for their formation, whereas loss of PC does not affect MRC function or formation. Unlike CL, mitochondrial PE or PC is not required for MRC supercomplex formation, emphasizing the specific requirement of CL in supercomplex assembly. Of interest, PE biosynthesized in the endoplasmic reticulum (ER) can functionally substitute for the lack of mitochondrial PE biosynthesis, suggesting the existence of PE transport pathway from ER to mitochondria. To understand the mechanism of PE transport, we disrupted ER–mitochondrial contact sites formed by the ERMES complex and found that, although not essential for PE transport, ERMES facilitates the efficient rescue of mitochondrial PE deficiency. Our work highlights specific roles of non–bilayer-forming phospholipids in MRC function and formation.

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