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The objectives of the present study were to explore how increased H<jats:sup>+<\/jats:sup> and K<jats:sup>+<\/jats:sup> fluxes influence heart mitochondrial physiology with regard to production and scavenging of reactive oxygen species (ROS), volume changes and resistance to calcium-induced mitochondrial permeability transition (mPT).<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Results<\/jats:title>\n            <jats:p>Isolated rat heart mitochondria were exposed to a wide concentration range of the protonophore CCCP or the potassium ionophore valinomycin to induce increased H<jats:sup>+<\/jats:sup> and K<jats:sup>+<\/jats:sup> conductance, respectively. Simultaneous monitoring of mitochondrial respiration and calcium retention capacity (CRC) demonstrated that the relative increase in respiration caused by valinomycin or CCCP correlated with a decrease in CRC, and that no level of respiratory uncoupling was associated with enhanced resistance to mPT. Mitochondria suspended in hyperosmolar buffer demonstrated a dose-dependent reduction in CRC with increasing osmolarity. However, mitochondria in hypoosmolar buffer to increase matrix volume did not display increased CRC. ROS generation was reduced by both K<jats:sup>+<\/jats:sup>- and H<jats:sup>+<\/jats:sup>-mediated respiratory uncoupling. The ability of heart mitochondria to detoxify H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub> was substantially greater than the production rate. The H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub> detoxification was dependent on respiratory substrates and was dramatically decreased following calcium-induced mPT, but was unaffected by uncoupling via increased K<jats:sup>+<\/jats:sup> and H<jats:sup>+<\/jats:sup> conductance.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Conclusion<\/jats:title>\n            <jats:p>It is concluded that respiratory uncoupling is not directly beneficial to rat heart mitochondrial resistance to calcium overload irrespective of whether H<jats:sup>+<\/jats:sup> or K<jats:sup>+<\/jats:sup> conductance is increased. The negative effects of respiratory uncoupling thus probably outweigh the reduction in ROS generation and a potential positive effect by increased matrix volume, resulting in a net sensitization of heart mitochondria to mPT activation.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1186\/1471-2121-14-40","type":"journal-article","created":{"date-parts":[[2013,9,28]],"date-time":"2013-09-28T17:01:48Z","timestamp":1380387708000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":6,"title":["Respiratory uncoupling by increased H+ or K+ flux is beneficial for heart mitochondrial turnover of reactive oxygen species but not for permeability transition"],"prefix":"10.1186","volume":"14","author":[{"given":"Saori","family":"Morota","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sarah","family":"Piel","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Magnus J","family":"Hansson","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"297","published-online":{"date-parts":[[2013,9,22]]},"reference":[{"key":"677_CR1","doi-asserted-by":"publisher","first-page":"1124","DOI":"10.1161\/01.CIR.74.5.1124","volume":"74","author":"CE Murry","year":"1986","unstructured":"Murry CE, Jennings RB, Reimer KA: Preconditioning with ischemia: a delay of lethal cell injury in ischemic myocardium. 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