ArticleExperimental and clinical cardiology2013
Substrate-dependent modulation of oxidative phosphorylation in isolated mitochondria following in vitro hypoxia and reoxygenation injury.
Article in Experimental and clinical cardiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Dexmedetomidine enables copper homeostasis in cerebral ischemia/reperfusion via ferredoxin 1.Annals of medicine · 2023Article
- Melatonin Mitigates Rotenone-Induced Oxidative Stress and Mitochondrial Dysfunction in theACS omega · 2023Article
- Metabolic Rewiring Is Essential for AML Cell Survival to Overcome Autophagy Inhibition by Loss of ATG3.Cancers · 2021Article
- Inorganic Polyphosphates As Storage for and Generator of Metabolic Energy in the Extracellular Matrix.Chemical reviews · 2019Review
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Authors and funding
5 authors.
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Abstract
BACKGROUND/
objectivesPrevious studies using isolated mitochondria have provided new insight into the mechanisms and interventions for ischemia and reperfusion (I/R) injury. In in vitro experiments involving isolated mitochondria, hypoxia and reoxygenation (H/R) has been widely used to mimic I/R injury. However, in in vitro H/R mitochondrial experiments, the effects of various substrates on mitochondrial oxidative phosphorylation are unclear. In the present study, the effects of in vitro I/R injury on mitochondrial oxidative phosphorylation under different substrate conditions were investigated.
methodsHypoxia was achieved following complete consumption of oxygen by mitochondria isolated from rat heart tissue in an experimental chamber. The H/R protocol involved 30 min hypoxia followed by 15 min reoxygenation in a chamber opened to the atmosphere. Mitochondrial respiration and respiratory control ratio (RCR) were measured.
resultsWhen pyruvate/malate were used as substrates, H/R significantly decreased state 3 respiration (28.2±12 nmol O2/min/mg protein) and RCR (2.7±0.8) compared with the control (121.4±32.5 nmol O2/mg protein/min and 7.8±1.2, respectively). In contrast, when succinate was used without rotenone, H/R significantly increased state 3 respiration (57.0±11.2 nmol O2/mg protein/min) and RCR (2.0±0.3) compared with the control (48.2±12.3 nmol O2/mg protein/min and 1.3±0.2, respectively).
conclusionsThe present study demonstrated that mitochondrial oxidative phosphorylation can be modulated by H/R in vitro depending on substrate conditions.
Indexed as
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23940443PMC3718598What OpenQuestion holds
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