Changes in oxygen tension affect cardiac mitochondrial respiration rate via changes in the rate of mitochondrial hydrogen peroxide production

Maria, Carla A.D.; Bogoyevitch, Marie A.; McKitrick, Douglas J.; Arnolda, Leonard F; Hool, Livia C.; Arthur, Peter G.

doi:10.1016/j.yjmcc.2009.03.010

Cited by 10 publications

(8 citation statements)

References 47 publications

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“… 10 , 11 Accordingly, both W21 and W50 models displayed an increased formation of 3-NT, a footprint of nitro-oxidative stress and more specifically peroxynitrite, a cytotoxic oxidant playing key pathogenic roles in reperfusion/reoxygenation injury. 25 In contrast, protein carbonyl adducts (marker of protein oxidative damage) increased only in W50 lungs, which is consistent with an enhanced flux of reactive oxidants from enzymes (eg, xanthine oxidase, NADPH oxidase) 26 , 27 and from the mitochondrial electron transport chain 28 at higher local PO 2 . Furthermore, W50 displayed considerably greater release of LDH, indicating that the higher FiO 2 promoted lung injury after WI.…”

Section: Discussionsupporting

confidence: 57%

Experimental Models of Ischemic Lung Damage for the Study of Therapeutic Reconditioning During Ex Vivo Lung Perfusion

Parapanov¹,

Wang²,

Wang³

et al. 2022

Transplantation Direct

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Background. Ex vivo lung perfusion (EVLP) may allow therapeutic reconditioning of damaged lung grafts before transplantation. This study aimed to develop relevant rat models of lung damage to study EVLP therapeutic reconditioning for possible translational applications. Methods. Lungs from 31 rats were exposed to cold ischemia (CI) or warm ischemia (WI), inflated at various oxygen fractions (FiO2), followed by 3 h EVLP. Five groups were studied as follow: (1) C21 (control): 3 h CI (FiO2 0.21); (2) C50: 3 h CI (FiO2 0.5); (3) W21: 1 h WI, followed by 2 h CI (FiO2 0.21); (4) W50: 1 h WI, followed by 2 h CI (FiO2 0.5); and (5) W2h: 2 h WI, followed by 1 h CI (FiO2 0.21). Following 3 h EVLP, we measured static pulmonary compliance (SPC), pulmonary vascular resistance, lung weight gain (edema), oxygenation capacity (differential partial pressure of oxygen), and protein carbonyls in lung tissue (oxidative stress), as well as lactate dehydrogenase (LDH, lung injury), nitrotyrosine (nitro-oxidative stress), interleukin-6 (IL-6, inflammation), and proteins (permeability edema) in bronchoalveolar lavage (BAL). Perivascular edema was quantified by histology. Results. No significant alterations were noted in C21 and C50 groups. W21 and W50 groups had reduced SPC and disclosed increased weight gain, BAL proteins, nitrotyrosine, and LDH. These changes were more severe in the W50 group, which also displayed greater oxidative stress. In contrast, both W21 and W50 showed comparable perivascular edema and BAL IL-6. In comparison with the other WI groups, W2h showed major weight gain, perivascular edema, SPC reduction, drop of differential partial pressure of oxygen, and massive increases of BAL LDH and proteins but comparable increase of IL-6 and biomarkers of oxidative stress. Conclusions. These models of lung damage of increasing severity might be helpful to evaluate new strategies for EVLP therapeutic reconditioning. A model combining 1 h WI and inflation at FiO2 of 0.5 seems best suited for this purpose by reproducing major alterations of clinical lung ischemia-reperfusion injury.

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Section: Discussionsupporting

confidence: 57%

Experimental Models of Ischemic Lung Damage for the Study of Therapeutic Reconditioning During Ex Vivo Lung Perfusion

Parapanov¹,

Wang²,

Wang³

et al. 2022

Transplantation Direct

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“…Recent experiments suggest that the mean mitochondrial PO 2 for Langendorff-perfused hearts is ~25mmHg, yet the major fraction of mitochondria are ~5mmHg [31], suggesting that our calculated values likely reflect PO 2 in the intact perfused heart. Furthermore, acute declines in mitochondrial PO 2 (10-13 mmHg) did not decrease the mitochondrial respiration rate, implying that this threshold is sufficient to support oxidative metabolism [32]. Indeed, previous observations suggest that oxidative phosphorylation requires similar oxygen tensions (12 mmHg) [33,34].…”

Section: Oxygen Kineticsmentioning

confidence: 82%

Changes to both cardiac metabolism and performance accompany acute reductions in functional capillary supply

Hui‐Kang

Winter

Alshammari

et al. 2015

Biochimica et Biophysica Acta (BBA) - General Subjects

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METHODS: Metabolism of substrates was measured before and after infusion of polystyrene microspheres in the perfused working heart to mimic random capillary loss due to microvascular disease. The effect of acute loss of functional capillary supply on palmitate and glucose metabolism together with function was quantified, and theoretical tissue oxygen distribution calculated from histological samples and ventricular VO 2 estimated.RESULTS: Microsphere infusion led to a dose-dependent decrease in rate-pressure product (RPP) and oxygen consumption (P<0.001). Microsphere infusion also increased work/unit oxygen consumption of hearts ('efficiency') by 25% (P<0.01). When corrected for cardiac work palmitate oxidation remained tightly coupled to very low workloads (RPP<2,500 mmHg/min), illustrating a high degree of metabolic control. Arteriole occlusion by microspheres decreased the density of patent capillaries (P<0.001) and correspondingly increased the average capillary supply area by 40% (P<0.01).Calculated rates of oxygen consumption declined from 16.6 ± 7.2 ml/100ml/min to 12.4 ± 9 ml/100ml/min following arteriole occlusion, coupled with increases in size of regions of myocardial hypoxia (Control = 22.0% vs. Microspheres = 42.2%).CONCLUSIONS: Cardiac mechanical performance is very sensitive to arteriolar blockade, but metabolite switching from fatty acid to glucose utilisation may also support cardiac function in regions of declining PO 2 .

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“…Interindividual or interpopulation differences in mitochondrial function (e.g., mitochondrial respiration) or COX activities have been considered as fitness-related traits in ectotherms, and their modification contributes to variation of metabolic rates (e.g., Ellison & Burton, 2006;Seebacher & Wilson, 2006;Speakman et al, 2004;White et al, 2012). The suppressed thermal sensitivity of mitochondrial metabolism in cold-acclimated T. wolteri matched well with the pattern in respiratory gas exchange at the whole-organism level, suggesting that actual energy turnover may be driven by liver mitochondrial capacities in this species, but not in the widespread temperate or tropical species (e.g., di Maria et al, 2009;White et al, 2012).…”

Section: Two Distinct Mechanisms Of Acclimationmentioning

confidence: 84%

Higher metabolic plasticity in temperate compared to tropical lizards suggests increased resilience to climate change

Sun

Williams

et al. 2022

Ecological Monographs

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Patterns in functional diversity of organisms at large spatial scales can provide insight into possible responses to future climate change, but it remains a challenge to link large-scale patterns at the population or species level to their underlying physiological mechanisms at the individual level. The climate variability hypothesis predicts that temperate ectotherms will be less vulnerable to climate warming compared with tropical ectotherms, due to their superior acclimatization capacity.However, metabolic acclimatization occurs over multiple levels, from the enzyme and cellular level, through organ systems, to whole-organism metabolic rate (from this point forwards biological hierarchy). Previous studies have focused on one or a few levels of the biological hierarchy, leaving us without a general understanding of how metabolic acclimatization might differ between tropical and temperate species. Here, we investigated thermal acclimation of three species of Takydromus lizards distributed along a broad latitudinal gradient in China, by studying metabolic modifications at the level of the whole organism, organ, mitochondria, metabolome, and proteome. As predicted by the climate variability hypothesis, the two temperate species T. septentrionalis and T. wolteri had an enhanced acclimation response at the whole organism level compared with the tropical species T. sexlineatus, as measured by respiratory gas exchange rates. However, the mechanisms by which whole organism performance was modified was strikingly different in the two temperate species: widespread T. septentrionalis modified organ sizes, whereas the narrowly distributed T. wolteri relied on mitochondrial, proteomic and metabolomic regulation. We suggest that these two mechanisms of thermal acclimatization may represent general strategies used by ectotherms, with distinct ecological costs and benefits. Lacking either of these mechanisms of thermal acclimatization capacity, the tropical species is likely to have increased vulnerability to climate change.

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Changes in oxygen tension affect cardiac mitochondrial respiration rate via changes in the rate of mitochondrial hydrogen peroxide production

Cited by 10 publications

References 47 publications

Experimental Models of Ischemic Lung Damage for the Study of Therapeutic Reconditioning During Ex Vivo Lung Perfusion

Experimental Models of Ischemic Lung Damage for the Study of Therapeutic Reconditioning During Ex Vivo Lung Perfusion

Changes to both cardiac metabolism and performance accompany acute reductions in functional capillary supply

Higher metabolic plasticity in temperate compared to tropical lizards suggests increased resilience to climate change

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