Light-Driven Oxygen Consumption in the Water-Water Cycles and Photorespiration, and Light Stimulated Mitochondrial Respiration

2020 ◽  
pp. 161-178 ◽  
Author(s):  
John A. Raven ◽  
John Beardall ◽  
Antonietta Quigg
Keyword(s):  
Oxygen Consumption ◽  
Mitochondrial Respiration ◽  
Water Cycles

scholarly journals Cell-Permeable Succinate Rescues Mitochondrial Respiration in Cellular Models of Statin Toxicity

2021 ◽  
Vol 22 (1) ◽  
pp. 424
Author(s):  
Vlad F. Avram ◽  
Imen Chamkha ◽  
Eleonor Åsander-Frostner ◽  
Johannes K. Ehinger ◽  
Romulus Z. Timar ◽  
...  
Keyword(s):  
Oxygen Consumption ◽  
Mitochondrial Dysfunction ◽  
Mitochondrial Respiration ◽  
Complex I ◽  
Ex Vivo ◽  
Coupling Efficiency ◽  
Human Platelets ◽  
Lipid Lowering ◽  
Lipid Lowering Therapy ◽  
Cellular Models

Statins are the cornerstone of lipid-lowering therapy. Although generally well tolerated, statin-associated muscle symptoms (SAMS) represent the main reason for treatment discontinuation. Mitochondrial dysfunction of complex I has been implicated in the pathophysiology of SAMS. The present study proposed to assess the concentration-dependent ex vivo effects of three statins on mitochondrial respiration in viable human platelets and to investigate whether a cell-permeable prodrug of succinate (complex II substrate) can compensate for statin-induced mitochondrial dysfunction. Mitochondrial respiration was assessed by high-resolution respirometry in human platelets, acutely exposed to statins in the presence/absence of the prodrug NV118. Statins concentration-dependently inhibited mitochondrial respiration in both intact and permeabilized cells. Further, statins caused an increase in non-ATP generating oxygen consumption (uncoupling), severely limiting the OXPHOS coupling efficiency, a measure of the ATP generating capacity. Cerivastatin (commercially withdrawn due to muscle toxicity) displayed a similar inhibitory capacity compared with the widely prescribed and tolerable atorvastatin, but did not elicit direct complex I inhibition. NV118 increased succinate-supported mitochondrial oxygen consumption in atorvastatin/cerivastatin-exposed platelets leading to normalization of coupled (ATP generating) respiration. The results acquired in isolated human platelets were validated in a limited set of experiments using atorvastatin in HepG2 cells, reinforcing the generalizability of the findings.

Effects of cocaine on oxygen consumption and mitochondrial respiration in normoxic and hypoxic mice

Life Sciences ◽  
1992 ◽  
Vol 50 (3) ◽  
pp. 213-218 ◽  
Author(s):  
Fabiola León-Velarde ◽  
Luis Huicho ◽  
Carlos Monge-C
Keyword(s):  
Oxygen Consumption ◽  
Mitochondrial Respiration

scholarly journals Chronic Hypoxia Enhances β-Oxidation-Dependent Electron Transport via Electron Transferring Flavoproteins

Cells ◽  
2019 ◽  
Vol 8 (2) ◽  
pp. 172 ◽  
Author(s):  
Dominik C. Fuhrmann ◽  
Catherine Olesch ◽  
Nina Kurrle ◽  
Frank Schnütgen ◽  
Sven Zukunft ◽  
...  
Keyword(s):  
Oxygen Consumption ◽  
Fatty Acid ◽  
Electron Transport ◽  
Mitochondrial Respiration ◽  
Chronic Hypoxia ◽  
Acute Hypoxia ◽  
Acid Synthesis ◽  
Acid Oxidation ◽  
Fatty Acid Production ◽  
Consumption Rates

Hypoxia poses a stress to cells and decreases mitochondrial respiration, in part by electron transport chain (ETC) complex reorganization. While metabolism under acute hypoxia is well characterized, alterations under chronic hypoxia largely remain unexplored. We followed oxygen consumption rates in THP-1 monocytes during acute (16 h) and chronic (72 h) hypoxia, compared to normoxia, to analyze the electron flows associated with glycolysis, glutamine, and fatty acid oxidation. Oxygen consumption under acute hypoxia predominantly demanded pyruvate, while under chronic hypoxia, fatty acid- and glutamine-oxidation dominated. Chronic hypoxia also elevated electron-transferring flavoproteins (ETF), and the knockdown of ETF–ubiquinone oxidoreductase lowered mitochondrial respiration under chronic hypoxia. Metabolomics revealed an increase in citrate under chronic hypoxia, which implied glutamine processing to α-ketoglutarate and citrate. Expression regulation of enzymes involved in this metabolic shunting corroborated this assumption. Moreover, the expression of acetyl-CoA carboxylase 1 increased, thus pointing to fatty acid synthesis under chronic hypoxia. Cells lacking complex I, which experienced a markedly impaired respiration under normoxia, also shifted their metabolism to fatty acid-dependent synthesis and usage. Taken together, we provide evidence that chronic hypoxia fuels the ETC via ETFs, increasing fatty acid production and consumption via the glutamine-citrate-fatty acid axis.

Mitochondrial respiration in muscle and liver from cold-acclimated hypothyroid rats

2003 ◽  
Vol 95 (4) ◽  
pp. 1584-1590 ◽  
Author(s):  
Angel A. Zaninovich ◽  
Inés Rebagliati ◽  
Marcela Raíces ◽  
Conrado Ricci ◽  
Karl Hagmüller
Keyword(s):  
Adipose Tissue ◽  
Oxygen Consumption ◽  
Brown Adipose Tissue ◽  
Cold Acclimation ◽  
Cold Exposure ◽  
Mitochondrial Respiration ◽  
Mitochondrial Oxygen Consumption ◽  
Normal Body ◽  
Thyroid Ablation ◽  
Brown Adipose

The effects of long-term cold exposure on muscle and liver mitochondrial oxygen consumption in hypothyroid and normal rats were examined. Thyroid ablation was performed after 8-wk acclimation to 4°C. Hypothyroid and normal controls remained in the cold for an additional 8 wk. At the end of 16-wk cold exposure, all hypothyroid rats were alive and normothermic and had normal body weight. At ambient temperature (24°C), thyroid ablation induced a 65% fall in muscle mitochondrial oxygen consumption, which was reversed by thyroxine but not by norepinephrine administration. After cold acclimation was reached, suppression of thyroid function reduced muscle mitochondrial respiration by 30%, but the hypothyroid values remained about threefold higher than those in hypothyroid muscle in the warm. Blockade of β- and α1-adrenergic receptors in both hypothyroid and normal rats produced hypothermia in vivo and a fall in muscle, liver, and brown adipose tissue mitochondria respiration in vitro. In normal rats, cold acclimation enhanced muscle respiration by 35%, in liver 18%, and in brown adipose tissue 450% over values in the warm. The results demonstrate that thyroid hormones, in the presence of norepinephrine, are major determinants of thermogenic activity in muscle and liver of cold-acclimated rats. After thyroid ablation, cold-induced nonshivering thermogenesis replaced 3,5,3′-triiodothyronine-induced thermogenesis, and normal body temperature was maintained.

scholarly journals Impaired Mitochondrial Bioenergetics Function in Pediatric Chronic Overlapping Pain Conditions with Functional Gastrointestinal Disorders

2021 ◽  
Vol 2021 ◽  
pp. 1-7
Author(s):  
Gisela Chelimsky ◽  
Pippa Simpson ◽  
Liyun Zhang ◽  
Doug Bierer ◽  
Steve Komas ◽  
...  
Keyword(s):  
Oxygen Consumption ◽  
Respiratory Chain ◽  
Mitochondrial Function ◽  
Mitochondrial Respiration ◽  
Functional Disability ◽  
Functional Gastrointestinal Disorders ◽  
Energy Generation ◽  
Proton Leak ◽  
Gastrointestinal Disorders ◽  
Reserve Capacity

Background. Fatigue is often the primary complaint of children with functional gastrointestinal disorders (FGDI) and other chronic overlapping pain disorders (COPC). The basis for this symptom remains unknown. We evaluated mitochondrial function in the white blood cells of these patients. Methods. This prospective Children’s Wisconsin IRB approved study recruited subjects aging 10–18 years from pediatric neurogastroenterology clinics and healthy comparison subjects (HC). Environmental and oxidative stressors can damage the mitochondrial respiratory chain. The known low-grade inflammation in COPC could, therefore, impact the respiratory chain and theoretically account for the disabling fatigue so often voiced by patients. Mitochondrial energy generation can be easily measured in peripheral mononuclear cells (PMC) as a general marker by the Seahorse XF96 Extracellular Flux Analyzer. We measured 5 parameters of oxygen consumption using this methodology: basal respiration (BR), ATP linked oxygen consumption (ATP-LC), maximal oxygen consumption rate (max R), spare respiratory capacity (SRC), and extracellular acidification rate (ECAR), which reflect non-electron chain energy generation through glycolysis. In health, we expect high ATP linked respiration, high reserve capacity, low proton leak, and low non-mitochondrial respiration. In disease, the proton leak typically increases, ATP demand increases, and there is decreased reserve capacity with increased non-mitochondrial respiration. Findings and clinical data were compared to healthy control subjects using a Mann–Whitney test for skewed variables, Fisher’s exact test for dichotomous variables, and regression tree for association with functional outcome (functional disability inventory, FDI). Results. 19 HC and 31 COPC showed no statistically significant difference in age. FGID, orthostatic intolerance, migraine, sleep disturbance, and chronic fatigue were present in the majority of COPC subjects. BR, ECAR, and ATP-LC rates were lower in the COPC group. The low BR and ATP-LC suggest that mitochondria are stressed with decreased ability to produce ATP. Tree analysis selected SRC as the best predictor of functional disability: patients with SRC >150 had a greater FDI (more disability) compared to patients with SRC <=150, p -value = 0.021. Conclusion. Subjects with COPC have reduced mitochondrial capacity to produce ATP. Predisposing genetic factors or reversible acquired changes may be responsible. A higher SRC best predicts disability. Since a higher SRC is typically associated with more mitochondrial reserve, the SRC may indicate an underutilized available energy supply related to inactivity, or a “brake” on mitochondrial function. Prospective longitudinal studies can likely discern whether these findings represent deconditioning, true mitochondrial dysfunction, or both.

scholarly journals REDUCED CITRATE SYNTHASE ACTIVITY EFFECT ON OXYGEN CONSUMPTION RATES IN ISOLATED MITOCHONDRIA FROM MICE LIVER AND MUSCLES

2016 ◽  
Vol 2 (101) ◽  
pp. 26-30
Author(s):  
Andrej Fokin ◽  
Rasa Žūkienė ◽  
Aivaras Ratkevičius
Keyword(s):  
Oxygen Consumption ◽  
Mitochondrial Respiration ◽  
Skeletal Muscles ◽  
Citrate Synthase ◽  
Oxygen Electrode ◽  
Isolated Mitochondria ◽  
Activity Effect ◽  
Consumption Rates ◽  
Centrifugation Method ◽  
Mice Liver

Background. Liver and skeletal muscles play the major role in metabolism. Mitochondria are of particular importance in functioning of these organs. We tested the hypothesis that reduced citrate synthase (CS) activity could induce improved fatty substrate and carbohydrate oxidation in mitochondria extracted from liver and hind limb muscles of mice. Methods. Eight mice each of 12-week-old control C57B6/J (B6) and congenic B6.A-(rs3676616-D10Utsw1)/ Kjn (B6.A) mice were studied. The mitochondria were isolated by differential centrifugation method followed by assessment of mitochondrial respiration and citrate synthase (CS) activity. Mitochondrial respiration was measured as oxygen consumption with Clark-type oxygen electrode by using polarography system. CS enzyme activity was measured spectrophotometrically. Results. The activity of CS was by ~32% lower for mitochondria for B6.A compared to B6 mice (603.9 ± 135.6 U/g and 894.2 ± 193.2 U/g, respectively). Mitochondrial respiration did not differ significantly between the strains. Conclusions. 30% reduction in citrate synthase activity does not impair mitochondrial respiration.

Effect of hyperthermia and acidosis on equine skeletal muscle mitochondrial oxygen consumption

2020 ◽  
pp. 1-10
Author(s):  
M.S. Davis ◽  
M.R. Fulton ◽  
A. Popken
Keyword(s):  
Skeletal Muscle ◽  
Oxygen Consumption ◽  
Oxidative Phosphorylation ◽  
Muscle Fatigue ◽  
Mitochondrial Function ◽  
Mitochondrial Respiration ◽  
Complex I ◽  
Mitochondrial Oxygen Consumption ◽  
Biochemical Basis ◽  
Complex Ii

The skeletal muscle of exercising horses develops pronounced hyperthermia and acidosis during strenuous or prolonged exercise, with very high tissue temperature and low pH associated with muscle fatigue or damage. The purpose of this study was to evaluate the individual effects of physiologically relevant hyperthermia and acidosis on equine skeletal muscle mitochondrial function, using ex vivo measurement of oxygen consumption to assess the function of different mitochondrial elements. Fresh triceps muscle biopsies from 6 healthy unfit Thoroughbred geldings were permeabilised to permit diffusion of small molecular weight substrates through the sarcolemma and analysed in a high resolution respirometer at 38, 40, 42, and 44 °C, and pH=7.1, 6.5, and 6.1. Oxygen consumption was measured under conditions of non-phosphorylating (leak) respiration and phosphorylating respiration through Complex I and Complex II. Data were analysed using a one-way repeated measures ANOVA and data are expressed as mean ± standard deviation. Leak respiration was ~3-fold higher at 44 °C compared to 38 °C regardless of electron source (Complex I: 22.88±3.05 vs 8.08±1.92 pmol O2/mg/s), P=0.002; Complex II: 79.14±23.72 vs 21.43±11.08 pmol O2/mg/s, P=0.022), resulting in a decrease in efficiency of oxidative phosphorylation. Acidosis had minimal effect on mitochondrial respiration at pH=6.5, but pH=6.1 resulted in a 50% decrease in mitochondrial oxygen consumption. These results suggest that skeletal muscle hyperthermia decreases the efficiency of oxidative phosphorylation through increased leak respiration, thus providing a specific biochemical basis for hyperthermia-induced muscle fatigue. The effect of myocellular acidosis on mitochondrial respiration was minimal under typical levels of acidosis, but atypically severe acidosis can lead to impairment of mitochondrial function.

scholarly journals Macrophages from the upper and lower human respiratory tract are metabolically distinct

2018 ◽  
Vol 315 (5) ◽  
pp. L752-L764 ◽  
Author(s):  
Katelyn S. Lavrich ◽  
Adam M. Speen ◽  
Andrew J. Ghio ◽  
Philip A. Bromberg ◽  
James M. Samet ◽  
...  
Keyword(s):  
Oxygen Consumption ◽  
Respiratory Tract ◽  
Mitochondrial Respiration ◽  
Ex Vivo ◽  
Air Pollutant ◽  
Induced Sputum ◽  
Blood Monocytes ◽  
Extracellular Acidification ◽  
Healthy Human ◽  
Lung Macrophages

The function and cell surface phenotype of lung macrophages vary within the respiratory tract. Alterations in the bioenergetic profile of macrophages may also be influenced by their location within the respiratory tract. This study sought to characterize the bioenergetic profile of macrophages sampled from different locations within the respiratory tract at baseline and in response to ex vivo xenobiotic challenge. Surface macrophages recovered from healthy volunteers by induced sputum and by bronchial and bronchoalveolar lavage were profiled using extracellular flux analyses. Oxygen consumption and extracellular acidification rates were measured at rest and after stimulation with lipopolysaccharide (LPS), phorbol 12-myristate 13-acetate (PMA), or 1,2-naphthoquinone (1,2-NQ). Oxygen consumption and extracellular acidification rates were highly correlated for all macrophage samples. Induced sputum macrophages had relatively higher oxygen consumption and extracellular acidification rates and were largely reliant on glycolysis. In contrast, bronchial fraction and bronchoalveolar macrophages depended more heavily on mitochondrial respiration. Bronchoalveolar macrophages showed elevated LPS-induced cytokine responses. Unlike their autologous peripheral blood monocytes, lung macrophages from any source did not display bioenergetic changes following LPS stimulation. The protein kinase C activator PMA did not affect mitochondrial respiration, whereas the air pollutant 1,2-NQ induced marked mitochondrial dysfunction in bronchoalveolar and bronchial fraction macrophages. The bioenergetic characteristics of macrophages from healthy individuals are dependent on their location within the respiratory tract. These findings establish a regional bioenergetic profile for macrophages from healthy human airways that serves as a reference for changes that occur in disease.

Mitochondrial respiration after sepsis and prolonged hypoxia

1998 ◽  
Vol 275 (1) ◽  
pp. L139-L144 ◽  
Author(s):  
David E. Taylor ◽  
Stephen P. Kantrow ◽  
Claude A. Piantadosi
Keyword(s):  
Oxygen Consumption ◽  
Oxygen Tension ◽  
Mitochondrial Respiration ◽  
Cecal Ligation ◽  
Liver Mitochondria ◽  
Hypoxic Exposure ◽  
Rat Liver Mitochondria ◽  
Dependent Behavior ◽  
Hypoxic Incubation ◽  
And Control

Recently, marked oxygen dependence of respiration by isolated mitochondria after exposure to prolonged hypoxia has been described. Because mitochondrial oxygen-dependent respiration could significantly influence oxygen consumption during critical illness, we sought to confirm the oxygen-dependent behavior of mitochondria. We hypothesized that mitochondria isolated during sepsis would exhibit increased oxygen dependence. We isolated rat liver mitochondria 16 h after cecal ligation and puncture and found a 30–40% greater oxygen uptake compared with control rats under state 3 conditions. Mitochondria incubated in deoxygenated buffer were studied for oxygen dependence at 10-min intervals for 90 min. Mitochondrial respiration after reoxygenation was stable over a 60-min period of hypoxia for control rats and decreased slightly for septic rats (10–15%). State 3 respiration was 10% lower when mitochondria were reoxygenated at low (15–25 Torr) versus high (90–100 Torr) and low (10–15 Torr) versus intermediate (40–45 Torr) oxygen tension. Oxygen consumption with ascorbate+ N, N, N′, N′-tetramethyl- p-phenylenediamine was 20% lower at low versus high oxygen tension. No increase in oxygen dependence was observed during 1 h of hypoxic incubation. Our data indicate only a modest oxygen dependence of respiration between 10 and 100 Torr, which is similar for septic and control mitochondria. Additionally, oxygen dependence did not increase significantly during a 1-h hypoxic exposure for well-coupled mitochondrial preparations.

scholarly journals β-Hydroxybutyrate is reduced in humans with obesity-related NAFLD and displays a dose-dependent effect on skeletal muscle mitochondrial respiration in vitro

2020 ◽  
Vol 319 (1) ◽  
pp. E187-E195 ◽  
Author(s):  
Jacob T. Mey ◽  
Melissa L. Erickson ◽  
Christopher L. Axelrod ◽  
William T. King ◽  
Chris A. Flask ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Oxygen Consumption ◽  
Insulin Sensitivity ◽  
Mitochondrial Respiration ◽  
Liver Fat ◽  
Whole Body ◽  
Fat Accumulation ◽  
Impaired Insulin ◽  
Hepatic Fat

Nonalcoholic fatty liver disease (NAFLD) is characterized by hepatic fat accumulation and impaired insulin sensitivity. Reduced hepatic ketogenesis may promote these pathologies, but data are inconclusive in humans and the link between NAFLD and reduced insulin sensitivity remains obscure. We investigated individuals with obesity-related NAFLD and hypothesized that β-hydroxybutyrate (βOHB; the predominant ketone species) would be reduced and related to hepatic fat accumulation and insulin sensitivity. Furthermore, we hypothesized that ketones would impact skeletal muscle mitochondrial respiration in vitro. Hepatic fat was assessed by 1H-MRS in 22 participants in a parallel design, case control study [Control: n = 7, age 50 ± 6 yr, body mass index (BMI) 30 ± 1 kg/m2; NAFLD: n = 15, age 57 ± 3 yr, BMI 35 ± 1 kg/m2]. Plasma assessments were conducted in the fasted state. Whole body insulin sensitivity was determined by the gold-standard hyperinsulinemic-euglycemic clamp. The effect of ketone dose (0.5–5.0 mM) on mitochondrial respiration was conducted in human skeletal muscle cell culture. Fasting βOHB, a surrogate measure of hepatic ketogenesis, was reduced in NAFLD (−15.6%, P < 0.01) and correlated negatively with liver fat ( r2 = 0.21, P = 0.03) and positively with insulin sensitivity ( r2 = 0.30, P = 0.01). Skeletal muscle mitochondrial oxygen consumption increased with low-dose ketones, attributable to increases in basal respiration (135%, P < 0.05) and ATP-linked oxygen consumption (136%, P < 0.05). NAFLD pathophysiology includes impaired hepatic ketogenesis, which is associated with hepatic fat accumulation and impaired insulin sensitivity. This reduced capacity to produce ketones may be a potential link between NAFLD and NAFLD-associated reductions in whole body insulin sensitivity, whereby ketone concentrations impact skeletal muscle mitochondrial respiration.

Sign in / Sign up

Export Citation Format

Share Document