These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Anoxia-reoxygenation alters H2O2 efflux and sensitivity of redox centers to copper in heart mitochondria.
    Author: Isei MO, Chinnappareddy N, Stevens D, Kamunde C.
    Journal: Comp Biochem Physiol C Toxicol Pharmacol; 2021 Oct; 248():109111. PubMed ID: 34146700.
    Abstract:
    Mitochondrial reactive oxygen species (ROS) have been implicated in organ damage caused by environmental stressors, prompting studies on the effect of oxygen deprivation and metal exposure on ROS metabolism. However, how anoxia and copper (Cu) jointly influence heart mitochondrial ROS metabolism is not understood. We used rainbow trout heart mitochondria to probe the effects of anoxia-reoxygenation and Cu on hydrogen peroxide (H2O2) emission during oxidation of palmitoylcarnitine (PC), succinate, or glutamate-malate. In addition, we examined the influence of anoxia-reoxygenation and Cu on site-specific H2O2 emission capacities and key antioxidant enzymes, glutathione peroxidase (GPx) and thioredoxin reductase (TrxR). Results showed that anoxia-reoxygenation suppressed H2O2 emission regardless of substrate type or duration of anoxia. Anoxia-reoxygenation reduced mitochondrial sensitivity to Cu during oxidation of succinate or glutamate-malate whereas high Cu concentration additively stimulated H2O2 emission in mitochondria oxidizing PC. Prolonged anoxia-reoxygenation stimulated H2O2 emission from sites OF and IF, inhibited emission from sites IQ, IIF and IIIQo, and disparately altered the sensitivity of the sites to Cu. Interestingly, anoxia-reoxygenation increased GPx and TrxR activities, more prominently when reoxygenation followed a short duration of anoxia. Cu did not alter GPx but reduced TrxR activity in normoxic and anoxic-reoxygenated mitochondria. Overall, our study revealed potential mechanisms that may reduce oxidative damage associated with anoxia-reoxygenation and Cu exposure in heart mitochondria. The increased and decreased H2O2 emission from NADH/NAD+ and QH2/Q isopotential sites, respectively, may represent a balance between H2O2 required for oxygen deprivation-induced signaling and prevention of ROS burst associated with anoxia-reoxygenation.
    [Abstract] [Full Text] [Related] [New Search]