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Cis\u20105 and Myr at pathological concentrations markedly reduced mitochondrial membrane potential (\u0394\u03a8<jats:sub>m<\/jats:sub>), matrix <jats:styled-content style=\"fixed-case\">NAD<\/jats:styled-content>(P)H pool, Ca<jats:sup>2+<\/jats:sup> retention capacity, <jats:styled-content style=\"fixed-case\">ADP<\/jats:styled-content>\u2010 (state 3) and carbonyl cyanide 3\u2010chlorophenyl hydrazine\u2010stimulated (uncoupled) respiration, and <jats:styled-content style=\"fixed-case\">ATP<\/jats:styled-content> generation. By contrast, these fatty acids increased resting (state 4) respiration (uncoupling effect) with the involvement of the adenine nucleotide translocator because carboxyatractyloside significantly attenuated the increased state 4 respiration provoked by Cis\u20105 and Myr. Furthermore, the classical inhibitors of mitochondrial permeability transition (<jats:styled-content style=\"fixed-case\">MPT<\/jats:styled-content>) pore cyclosporin A plus <jats:styled-content style=\"fixed-case\">ADP<\/jats:styled-content>, as well as the Ca<jats:sup>2+<\/jats:sup> uptake blocker ruthenium red, fully prevented the Cis\u20105\u2010 and Myr\u2010induced decrease in \u0394\u03a8<jats:sub>m<\/jats:sub> in Ca<jats:sup>2+<\/jats:sup>\u2010loaded mitochondria, suggesting, respectively, the induction of <jats:styled-content style=\"fixed-case\">MPT<\/jats:styled-content> pore opening and the contribution of Ca<jats:sup>2+<\/jats:sup> toward these effects. The findings of the present study indicate that the major long\u2010chain fatty acids that accumulate in <jats:styled-content style=\"fixed-case\">VLCAD<\/jats:styled-content> deficiency disrupt mitochondrial bioenergetics and Ca<jats:sup>2+<\/jats:sup> homeostasis, acting as uncouplers and metabolic inhibitors of oxidative phosphorylation, as well as inducers of <jats:styled-content style=\"fixed-case\">MPT<\/jats:styled-content> pore opening, in the heart at pathological relevant concentrations. It is therefore presumed that a disturbance of bioenergetics and Ca<jats:sup>2+<\/jats:sup> homeostasis may contribute to the cardiac manifestations observed in <jats:styled-content style=\"fixed-case\">VLCAD<\/jats:styled-content> deficiency.<\/jats:p>","DOI":"10.1111\/febs.14419","type":"journal-article","created":{"date-parts":[[2018,2,24]],"date-time":"2018-02-24T13:11:13Z","timestamp":1519477873000},"page":"1437-1455","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":24,"title":["Metabolite accumulation in <scp>VLCAD<\/scp> deficiency markedly disrupts mitochondrial bioenergetics and Ca<sup>2+<\/sup> homeostasis in the heart"],"prefix":"10.1111","volume":"285","author":[{"given":"Cristiane","family":"Cecatto","sequence":"first","affiliation":[{"name":"Programa de P\u00f3s\u2010Gradua\u00e7\u00e3o em Ci\u00eancias Biol\u00f3gicas: Bioqu\u00edmica Instituto de Ci\u00eancias B\u00e1sicas da Sa\u00fade Universidade Federal do 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