Polarographic determination of mitochondrial respiration in Gastrothylax crumenifer

1987 ◽  
Vol 61 (2) ◽  
pp. 143-145
Author(s):  
Jawed Siddiqui ◽  
Ather H Siddiqi
Keyword(s):  
Oxygen Consumption ◽  
Oxidative Phosphorylation ◽  
Oxidative Metabolism ◽  
Mitochondrial Respiration ◽  
Mitochondrial Atpase ◽  
Mitochondrial Oxygen Consumption ◽  
Salicylhydroxamic Acid ◽  
Gastrothylax Crumenifer ◽  
Mitochondrial Fractions

ABSTRACTThe oxidative metabolism of Gastrothylax crumenifer mitochondrial fractions was assayed polarographically at 30°C in the presence of various substrates. Succinate was most readily oxidized, malate and pyruvate were oxidized at subsantially lower retes. The spcific inhibitors such as malonate, KCN, NaN3, oxaloacetate, salicylhydroxamic acid and oligomycin effectively affected the mitochondrial oxygen consumption. The results indicate the presence of oxidative phosphorylation and cytochrome systems. Mitochondrial ATPase was found to be active.

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.

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 The Role of Dietary Saturated Fat in Associations between Exposure to Ambient Fine Particulate Matter and Mitochondrial Respiratory Functions in Circulating Platelets

2021 ◽  
Vol 5 (Supplement_2) ◽  
pp. 523-523
Author(s):  
Wan Shen ◽  
Hao Chen ◽  
James Samet ◽  
Haiyan Tong
Keyword(s):  
Oxygen Consumption ◽  
Mitochondrial Respiration ◽  
Saturated Fatty Acids ◽  
Fine Particulate Matter ◽  
Saturated Fat ◽  
Basal Respiration ◽  
Mitochondrial Oxygen Consumption ◽  
Atp Production ◽  
Consumption Rates ◽  
Mitochondrial Respiratory

Abstract Objectives Exposure to ambient fine particulate matter (PM2.5) is associated with platelet activation and increased mitochondrial respiration. The impact of dietary saturated fat on the circulating platelets is not understood. This project aimed to determine whether dietary saturated fatty acids moderate mitochondrial respiratory function in circulating platelets after short-term exposure to PM2.5. Methods Platelets were isolated from 22 healthy male volunteers (mean age ± SD, 37 ± 8.2) in a panel study and measured for mitochondrial oxygen consumption rates using an extracellular flux analyzer. Intakes of saturated fat were determined from 24 hr dietary recalls the day before the assay. Daily ambient PM2.5 concentrations during the study period were obtained from ambient air quality monitoring stations. Data were fitted with a moderation model, where the level of ambient PM2.5 was the independent variable, saturated fat intake was the moderator, and mitochondrial respiratory functions in circulating platelets were the dependent variables. Results After controlling for age, dietary consumption of saturated fat moderated the mitochondrial oxygen consumption rates of non-mitochondrial respiration, basal respiration, maximum respiration, ATP production, and spare respiratory capacity after exposure to ambient PM2.5 with 2 days lag. Specifically, the negative associations between the above mentioned mitochondrial respiratory measurements and PM2.5 levels reached statistical significance (95% Confident Intervals did not include 0) in subjects with a high intake of total saturated fat. Further, results for individual saturated fatty acid showed similar patterns, specifically that negative association between mitochondrial oxygen consumption rates of non-mitochondrial respiration, basal respiration and ATP production and levels of exposed PM2.5 was moderated by intakes of short-chain (C4:0), medium-chain (C6:0, C8:0, C10:0, C12:0), long-chain (C14:0, C16:0) saturated fatty acids. Conclusions Taken together, these preliminary findings suggest that consumption of saturated fat moderates platelet mitochondrial respiration after exposure to PM2.5.  THIS ABSTRACT OF A PROPOSED PRESENTATION DOES NOT NECESSARILY REFLECT EPA POLICY. Funding Sources This project was supported by the U.S. EPA Intramural Research Program.

scholarly journals Relationship between Liver Mitochondrial Respiration and Proton Leak in Low and High RFI Steers from Two Lineages of RFI Angus Bulls

2015 ◽  
Vol 2015 ◽  
pp. 1-5 ◽  
Author(s):  
G. Acetoze ◽  
K. L. Weber ◽  
J. J. Ramsey ◽  
H. A. Rossow
Keyword(s):  
Body Weight ◽  
Oxygen Consumption ◽  
Mitochondrial Respiration ◽  
Dry Matter ◽  
Genetic Test ◽  
Bodyweight Gain ◽  
Dry Matter Intake ◽  
Proton Leak ◽  
Adaptation Period ◽  
Mitochondrial Oxygen Consumption

The objective of this research is to evaluate liver mitochondrial oxygen consumption and proton leak kinetics in progeny from two lineages of Angus bulls with high and low residual feed intake (RFI). Two Angus bulls were selected based on results from a genetic test for RFI and were used as sires. Eight offspring at 10-11 months of age from each sire were housed in individual pens for 70–105 days following a diet adaptation period of 14 days. Progeny of the low RFI sire had 0.57 kg/d (P=0.05) lower average RFI than progeny of the high RFI sire. There was no difference in dry matter intake between low and high RFI steers, but low RFI steers gained more body weight (P=0.02) and tended to have higher average daily gains (P=0.07). State 3 and State 4 respiration, RCR, and proton leak did not differ between high and low RFI steers (P=0.96, P=0.81, P=0.93, and P=0.88, resp.). Therefore, the increase in bodyweight gain which distinguished the low RFI steers from the high RFI steers may be associated with other metabolic mechanisms that are not associated with liver mitochondrial respiration and proton leak kinetics.

Quantification of the kinetic differences between communities isolated from completely mixed activated sludge systems operated with or without a selector using a novel respirometric method

1994 ◽  
Vol 30 (11) ◽  
pp. 255-261 ◽  
Author(s):  
Barth F. Smets ◽  
Timothy G. Ellis ◽  
Stephanie Brau ◽  
Richard W. Sanders ◽  
C. P. Leslie Grady
Keyword(s):  
Oxygen Consumption ◽  
Activated Sludge ◽  
Physiological Changes ◽  
Biodegradation Kinetics ◽  
Substrate Removal ◽  
Biomass Yields ◽  
Selection For ◽  
Single Oxygen ◽  
Activated Sludge Systems

This study quantified the kinetic differences in microbial communities isolated from completely mixed activated sludge (CMAS) systems that were operated either with or without an aerobic selector preceding the main reactor. A new respirometric method was employed that allowed the determination of biodegradation kinetics from single oxygen consumption curves, thereby minimizing physiological changes to the examined communities during the assay. Results indicated that increased values for Ks and μmax for acetate, phenol, and 4-chlorophenol degradation were measured in the CMAS system operated with a selector. The biomass yields on acetate, phenol, and 4-chlorophenol were very similar in both systems. These findings indicate that the operation of CMAS systems with aerobic selectors may result in the selection for degrading populations with higher Ks and μmax values for both biogenic and xenobiotic organic compounds, and that substrate storage in the selector only partially contributes to increased substrate removal rates.

scholarly journals Upregulation of COX4-2 via HIF-1α in Mitochondrial COX4-1 Deficiency

Cells ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 452
Author(s):  
Liza Douiev ◽  
Chaya Miller ◽  
Shmuel Ruppo ◽  
Hadar Benyamini ◽  
Bassam Abu-Libdeh ◽  
...  
Keyword(s):  
Oxygen Consumption ◽  
Oxidative Phosphorylation ◽  
Nuclear Localization ◽  
Target Genes ◽  
Compensatory Mechanism ◽  
Terminal Electron Acceptor ◽  
Human Foreskin Fibroblasts ◽  
Mitochondrial Respiratory Complex ◽  
Mrna Transcripts ◽  
Oxphos System

Cytochrome-c-oxidase (COX) subunit 4 (COX4) plays important roles in the function, assembly and regulation of COX (mitochondrial respiratory complex 4), the terminal electron acceptor of the oxidative phosphorylation (OXPHOS) system. The principal COX4 isoform, COX4-1, is expressed in all tissues, whereas COX4-2 is mainly expressed in the lungs, or under hypoxia and other stress conditions. We have previously described a patient with a COX4-1 defect with a relatively mild presentation compared to other primary COX deficiencies, and hypothesized that this could be the result of a compensatory upregulation of COX4-2. To this end, COX4-1 was downregulated by shRNAs in human foreskin fibroblasts (HFF) and compared to the patient’s cells. COX4-1, COX4-2 and HIF-1α were detected by immunocytochemistry. The mRNA transcripts of both COX4 isoforms and HIF-1 target genes were quantified by RT-qPCR. COX activity and OXPHOS function were measured by enzymatic and oxygen consumption assays, respectively. Pathways were analyzed by CEL-Seq2 and by RT-qPCR. We demonstrated elevated COX4-2 levels in the COX4-1-deficient cells, with a concomitant HIF-1α stabilization, nuclear localization and upregulation of the hypoxia and glycolysis pathways. We suggest that COX4-2 and HIF-1α are upregulated also in normoxia as a compensatory mechanism in COX4-1 deficiency.

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