scholarly journals Effects of variable oxygen regimes on mitochondrial bioenergetics and reactive oxygen species production in a marine bivalve, Mya arenaria

2021 ◽  
Vol 224 (4) ◽  
pp. jeb237156
Author(s):  
Natascha Ouillon ◽  
Eugene P. Sokolov ◽  
Stefan Otto ◽  
Gregor Rehder ◽  
Inna M. Sokolova
Keyword(s):  
Reactive Oxygen Species ◽  
Chronic Hypoxia ◽  
Coupling Efficiency ◽  
Oxygen Affinity ◽  
Reactive Oxygen ◽  
Mya Arenaria ◽  
Proton Leak ◽  
Marine Bivalve ◽  
Oxygen Species ◽  
Oxygen Levels

ABSTRACTEstuarine and coastal benthic organisms often experience fluctuations in oxygen levels that can negatively impact their mitochondrial function and aerobic metabolism. To study these impacts, we exposed a common sediment-dwelling bivalve, the soft-shell clam Mya arenaria, for 21 days to chronic hypoxia (PO2 ∼4.1 kPa), cyclic hypoxia (PO2 ∼12.7–1.9 kPa, mean 5.7 kPa) or normoxia (PO2 ∼21.1 kPa). pH was manipulated to mimic the covariation in CO2/pH and oxygen levels in coastal hypoxic zones. Mitochondrial respiration, including proton leak, the capacity for oxidative phosphorylation (OXPHOS), the maximum activity of the electron transport system (ETS), reactive oxygen species (ROS) production, and activity and oxygen affinity of cytochrome c oxidase (CCO) were assessed. Acclimation to constant hypoxia did not affect the studied mitochondrial traits except for a modest decrease in the OXPHOS coupling efficiency. Cyclic hypoxia had no effect on OXPHOS or ETS capacity, but increased proton leak and lowered mitochondrial OXPHOS coupling efficiency. Furthermore, mitochondria of clams acclimated to cyclic hypoxia had higher rates of ROS generation compared with the clams acclimated to normoxia or chronic hypoxia. CCO activity was upregulated under cyclic hypoxia, but oxygen affinity of CCO did not change. These findings indicate that long-term cyclic hypoxia has a stronger impact on the mitochondria of M. arenaria than chronic hypoxia and might lead to impaired ATP synthesis, higher costs of mitochondrial maintenance and oxidative stress. These changes might negatively affect populations of M. arenaria in the coastal Baltic Sea under increasing hypoxia pressure.

Proton leak induced by reactive oxygen species produced during in vitro anoxia/reoxygenation in rat skeletal muscle mitochondria

2006 ◽  
Vol 38 (1) ◽  
pp. 23-32 ◽  
Author(s):  
Rachel Navet ◽  
Ange Mouithys-Mickalad ◽  
Pierre Douette ◽  
Claudine M. Sluse-Goffart ◽  
Wieslawa Jarmuszkiewicz ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Skeletal Muscle ◽  
Reactive Oxygen ◽  
Proton Leak ◽  
Oxygen Species ◽  
Rat Skeletal Muscle ◽  
Muscle Mitochondria ◽  
Skeletal Muscle Mitochondria

Effects of short- and medium-term calorie restriction on muscle mitochondrial proton leak and reactive oxygen species production

2004 ◽  
Vol 286 (5) ◽  
pp. E852-E861 ◽  
Author(s):  
Lisa Bevilacqua ◽  
Jon J. Ramsey ◽  
Kevork Hagopian ◽  
Richard Weindruch ◽  
Mary-Ellen Harper
Keyword(s):  
Reactive Oxygen Species ◽  
Oxidative Phosphorylation ◽  
Metabolic Control ◽  
Calorie Restriction ◽  
Reactive Oxygen ◽  
Proton Leak ◽  
Ros Production ◽  
Oxygen Species ◽  
Medium Term ◽  
Time Points

Reductions in cellular oxygen consumption (V̇o2) and reactive oxygen species (ROS) production have been proposed as mechanisms underlying the anti-aging effects of calorie restriction (CR). Mitochondria are a cell's greatest “sink” for oxygen and also its primary source of ROS. The mitochondrial proton leak pathway is responsible for 20–30% of V̇o2 in resting cells. We hypothesized that CR leads to decreased proton leak with consequential decreases in V̇o2, ROS production, and cellular damage. Here, we report the effects of short-term (2-wk, 2-mo) and medium-term (6-mo) CR (40%) on rat muscle mitochondrial proton leak, ROS production, and whole animal V̇o2. Whole body V̇o2 decreased with CR at all time points, whereas mass-adjusted V̇o2 was normal until the 6-mo time point, when it was 40% lower in CR compared with control rats. At all time points, maximal leak-dependent V̇o2 was lower in CR rats compared with controls. Proton leak kinetics indicated that mechanisms of adaptation to CR were different between short- and medium-term treatments, with the former leading to decreases in protonmotive force (Δp) and state 4 V̇o2 and the latter to increases in Δp and decreases in state 4 V̇o2. Results from metabolic control analyses of oxidative phosphorylation are consistent with the idea that short- and medium-term responses are distinct. Mitochondrial H2O2 production was lower in all three CR groups compared with controls. Overall, this study details the rapid effects of short- and medium-term CR on proton leak, ROS production, and metabolic control of oxidative phosphorylation. Results indicate that a reduction in mitochondrial V̇o2 and ROS production may be a mechanism for the actions of CR.

scholarly journals Mitochondrial capacity and reactive oxygen species production during hypoxia and reoxygenation in the ocean quahog, Arctica islandica

2021 ◽  
Author(s):  
Jennifer B. M. Steffen ◽  
Fouzia Haider ◽  
Eugene P. Sokolov ◽  
Christian Bock ◽  
Inna M. Sokolova
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Substrate Oxidation ◽  
Hypoxia Tolerance ◽  
Oxygen Flux ◽  
Proton Leak ◽  
Control Analysis ◽  
Oxygen Species ◽  
Arctica Islandica ◽  
Normoxic Control

Oxygen fluctuations are common in marine waters, and hypoxia/reoxygenation (H/R) stress can negatively affect mitochondrial metabolism. The long-lived ocean quahog, Arctica islandica, is known for its hypoxia tolerance associated with metabolic rate depression, yet the mechanisms that sustain mitochondrial function during oxygen fluctuations are not well understood. We used top-down metabolic control analysis (MCA) to determine aerobic capacity and control over oxygen flux in the mitochondria of quahogs exposed to short-term hypoxia (24 h <0.01% O­2) and subsequent reoxygenation (1.5 h 21% O­2) compared to normoxic control animals (21% O­2). We demonstrated that flux capacities of the substrate oxidation and proton leak subsystems were not affected by hypoxia, while the capacity of the phosphorylation subsystem was enhanced during hypoxia associated with a depolarization of the mitochondrial membrane. Reoxygenation decreased oxygen flux capacities of all three mitochondrial subsystems. Control over oxidative phosphorylation (OXPHOS) respiration was mostly exerted by substrate oxidation regardless of H/R stress, whereas the control of the proton leak subsystem over LEAK respiration increased during hypoxia and returned to normoxic level during reoxygenation. During hypoxia, reactive oxygen species (ROS) efflux was elevated in the LEAK state, while suppressed in the OXPHOS state. Mitochondrial ROS efflux returned to normoxic control levels during reoxygenation. Thus, mitochondria of A. islandica appear robust to hypoxia by maintaining stable substrate oxidation and upregulating phosphorylation capacity, but remain sensitive to reoxygenation. This mitochondrial phenotype might reflect adaptation of A. islandica to environments with unpredictable oxygen fluctuations and its behavioural preference for low oxygen levels.

scholarly journals Reactive Oxygen Species Production in the Early and Later Stage of Chronic Ventilatory Hypoxia

2012 ◽  
pp. 145-151 ◽  
Author(s):  
D. HODYC ◽  
E. JOHNSON ◽  
A. SKOUMALOVÁ ◽  
J. TKACZYK ◽  
H. MAXOVÁ ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Pulmonary Hypertension ◽  
Chronic Hypoxia ◽  
Reactive Oxygen ◽  
No Production ◽  
Oxygen Species ◽  
Air Plasma ◽  
Species Production ◽  
Specific Timing

Pulmonary hypertension resulting from chronic hypoxia is at least partly caused by the increased production of reactive oxygen species (ROS). The goal of the presented study was to investigate the dynamics and the site of production of ROS during chronic hypoxia. In our study Wistar rats were kept for 1, 4 and 21 days in an isobaric hypoxic chamber (FiO2=0.1), while controls stayed in normoxia. We compared NO production in expired air, plasma and perfusate drained from isolated rat lungs and measured superoxide concentration in the perfusate. We also detected the presence of superoxide products (hydrogen peroxide and peroxynitrite) and the level of ROS-induced damage expressed as the concentration of lipid peroxydation end products. We found that the production and release of ROS and NO during early phase of chronic hypoxia has specific timing and differs in various compartments, suggesting the crucial role of ROS interaction for development of hypoxic pulmonary hypertension.

scholarly journals NADPH oxidases and reactive oxygen species at different stages of chronic hypoxia-induced pulmonary hypertension in newborn piglets

2009 ◽  
Vol 297 (4) ◽  
pp. L596-L607 ◽  
Author(s):  
Kathleen E. Dennis ◽  
J. L. Aschner ◽  
D. Milatovic ◽  
J. W. Schmidt ◽  
M. Aschner ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Pulmonary Hypertension ◽  
Chronic Hypoxia ◽  
Oxidant Stress ◽  
Reactive Oxygen ◽  
Gas Chromatography Mass Spectrometry ◽  
Oxygen Species ◽  
Resistance Arteries ◽  
Newborn Piglets ◽  
Air Control

Recently, we reported that reactive oxygen species (ROS) generated by NADPH oxidase (NOX) contribute to aberrant responses in pulmonary resistance arteries (PRAs) of piglets exposed to 3 days of hypoxia ( Am J Physiol Lung Cell Mol Physiol 295: L881–L888, 2008). An objective of the present study was to determine whether NOX-derived ROS also contribute to altered PRA responses at a more advanced stage of pulmonary hypertension, after 10 days of hypoxia. We further wished to advance knowledge about the specific NOX and antioxidant enzymes that are altered at early and later stages of pulmonary hypertension. Piglets were raised in room air (control) or hypoxia for 3 or 10 days. Using a cannulated artery technique, we found that treatments with agents that inhibit NOX (apocynin) or remove ROS [an SOD mimetic (M40403) + polyethylene glycol-catalase] diminished responses to ACh in PRAs from piglets exposed to 10 days of hypoxia. Western blot analysis showed an increase in expression of NOX1 and the membrane fraction of p67phox. Expression of NOX4, SOD2, and catalase were unchanged, whereas expression of SOD1 was reduced, in arteries from piglets raised in hypoxia for 3 or 10 days. Markers of oxidant stress, F2-isoprostanes, measured by gas chromatography-mass spectrometry, were increased in PRAs from piglets raised in hypoxia for 3 days, but not 10 days. We conclude that ROS derived from some, but not all, NOX family members, as well as alterations in the antioxidant enzyme SOD1, contribute to aberrant PRA responses at an early and a more progressive stage of chronic hypoxia-induced pulmonary hypertension in newborn piglets.

scholarly journals Pulmonary Arterial Responses to Reactive Oxygen Species Are Altered in Newborn Piglets With Chronic Hypoxia-Induced Pulmonary Hypertension

2011 ◽  
Vol 70 (2) ◽  
pp. 136-141 ◽  
Author(s):  
Candice D Fike ◽  
Judy L Aschner ◽  
James C Slaughter ◽  
Mark R Kaplowitz ◽  
Yongmei Zhang ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Pulmonary Hypertension ◽  
Chronic Hypoxia ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Newborn Piglets ◽  
Pulmonary Arterial ◽  
Arterial Responses

scholarly journals Temperature-dependence of mitochondrial function and production of reactive oxygen species in the intertidal mud clam Mya arenaria

2002 ◽  
Vol 205 (13) ◽  
pp. 1831-1841 ◽  
Author(s):  
D. Abele ◽  
K. Heise ◽  
H. O. Pörtner ◽  
S. Puntarulo
Keyword(s):  
Reactive Oxygen Species ◽  
Heat Stress ◽  
Heat Exposure ◽  
Reactive Oxygen ◽  
Mya Arenaria ◽  
Oxygen Species ◽  
Mitochondrial Ros ◽  
Ros Formation ◽  
Proton Leakage ◽  
Intertidal Population

SUMMARY Mitochondrial respiration, energetic coupling to phosphorylation and the production of reactive oxygen species (ROS) were studied in mitochondria isolated from the eurythermal bivalve Mya arenaria (Myoidea) from a low-shore intertidal population of the German Wadden Sea. Measurements were conducted both within the range of the habitat temperatures (5-15 °C) and when subjected to heat exposure at 20 °C and 25 °C. Experimental warming resulted in an increase in the rate of state 3 and state 4 respiration in isolated mitochondria. The highest respiratory coupling ratios (RCR) were found at 15 °C; at higher temperatures mitochondrial coupling decreased,and release of ROS doubled between 15 and 25 °C. ROS production was 2-3%of total oxygen consumption in state 3 (0.3-0.5 nmol ROS mg-1protein min-1) at the habitat temperature, reaching a maximum of 4.3 % of state 3 respiration and 7 % of oligomycin-induced state 4+respiration under heat stress. Thus, state 4 respiration, previously interpreted exclusively as a measure of proton leakage, included a significant contribution from ROS formation in this animal, especially under conditions of heat stress. Oxygen radical formation was directly dependent on temperature-controlled respiration rates in states 3 and 4 and inversely related to mitochondrial coupling (RCR+) in state 4. Mitochondrial ROS formation is therefore involved in cellular heat stress in this eurythermal marine ectotherm.

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