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Low production of mitochondrial reactive oxygen species after anoxia and reoxygenation in turtle hearts.

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Τίτλος: Low production of mitochondrial reactive oxygen species after anoxia and reoxygenation in turtle hearts.
Συγγραφείς: Bundgaard A; CECAD, University of Cologne, 50931 Cologne, Germany.; Department of Biology, Aarhus University, DK-8000 Aarhus, Denmark., Gruszczyk AV; MRC Mitochondrial Biology Unit, University of Cambridge, Cambridge CB2 0XY, UK., Prag HA; MRC Mitochondrial Biology Unit, University of Cambridge, Cambridge CB2 0XY, UK., Williams C; Department of Biology, Aarhus University, DK-8000 Aarhus, Denmark., McIntyre A; MRC Mitochondrial Biology Unit, University of Cambridge, Cambridge CB2 0XY, UK., Ruhr IM; Faculty of Medical and Human Sciences, University of Manchester, Manchester M13 9PL, UK., James AM; MRC Mitochondrial Biology Unit, University of Cambridge, Cambridge CB2 0XY, UK., Galli GLJ; Faculty of Medical and Human Sciences, University of Manchester, Manchester M13 9PL, UK., Murphy MP; MRC Mitochondrial Biology Unit, University of Cambridge, Cambridge CB2 0XY, UK., Fago A; Department of Biology, Aarhus University, DK-8000 Aarhus, Denmark.
Πηγή: The Journal of experimental biology [J Exp Biol] 2023 May 01; Vol. 226 (9). Date of Electronic Publication: 2023 May 10.
Τύπος έκδοσης: Journal Article; Research Support, Non-U.S. Gov't
Γλώσσα: English
Στοιχεία περιοδικού: Publisher: Company Of Biologists Limited Country of Publication: England NLM ID: 0243705 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1477-9145 (Electronic) Linking ISSN: 00220949 NLM ISO Abbreviation: J Exp Biol Subsets: MEDLINE
Imprint Name(s): Publication: London : Company Of Biologists Limited
Original Publication: London, Cambridge Univ. Press.
Ιατρικοί όροι (MeSH): Turtles*/metabolism, Reactive Oxygen Species/metabolism ; Superoxides/metabolism ; Hydrogen Peroxide/metabolism ; Hypoxia/metabolism ; Mitochondria, Heart/metabolism ; Succinic Acid/metabolism ; Succinates/metabolism ; Mammals/metabolism ; Animals
Περίληψη: Extremely anoxia-tolerant animals, such as freshwater turtles, survive anoxia and reoxygenation without sustaining tissue damage to their hearts. In contrast, for mammals, the ischemia-reperfusion (IR) injury that leads to tissue damage during a heart attack is initiated by a burst of superoxide (O2·-) production from the mitochondrial respiratory chain upon reperfusion of ischemic tissue. Whether turtles avoid oxidative tissue damage because of an absence of mitochondrial superoxide production upon reoxygenation, or because the turtle heart is particularly protected against this damage, is unclear. Here, we investigated whether there was an increase in mitochondrial O2·- production upon the reoxygenation of anoxic red-eared slider turtle hearts in vivo and in vitro. This was done by measuring the production of H2O2, the dismutation product of O2·-, using the mitochondria-targeted mass-spectrometric probe in vivo MitoB, while in parallel assessing changes in the metabolites driving mitochondrial O2·- production, succinate, ATP and ADP levels during anoxia, and H2O2 consumption and production rates of isolated heart mitochondria. We found that there was no excess production of in vivo H2O2 during 1 h of reoxygenation in turtles after 3 h anoxia at room temperature, suggesting that turtle hearts most likely do not suffer oxidative injury after anoxia because their mitochondria produce no excess O2·- upon reoxygenation. Instead, our data support the conclusion that both the low levels of succinate accumulation and the maintenance of ADP levels in the anoxic turtle heart are key factors in preventing the surge of O2·- production upon reoxygenation.
(© 2023. Published by The Company of Biologists Ltd.)
Competing Interests: Competing interests The authors declare no competing or financial interests.
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Grant Information: MC_UU_00028/4 United Kingdom MRC_ Medical Research Council; 220257/Z/20/Z United Kingdom WT_ Wellcome Trust
Contributed Indexing: Keywords: Trachemys scripta; Anoxia; Heart; Hibernation; Mitochondria; Oxidative damage; Reverse electron transfer
Substance Nomenclature: 0 (Reactive Oxygen Species)
11062-77-4 (Superoxides)
BBX060AN9V (Hydrogen Peroxide)
AB6MNQ6J6L (Succinic Acid)
0 (Succinates)
Entry Date(s): Date Created: 20230417 Date Completed: 20230511 Latest Revision: 20231111
Update Code: 20260130
PubMed Central ID: PMC10184768
DOI: 10.1242/jeb.245516
PMID: 37066839
Βάση Δεδομένων: MEDLINE
Περιγραφή
ISSN:1477-9145
DOI:10.1242/jeb.245516