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. 2020 May 7;17:15. doi: 10.1186/s12989-020-00346-2

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© The Author(s) 2020

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 6 — nanoSiO₂ induces an increase in mitochondrial ROS production, leading to dysfunction in cardiac contractility. Hearts perfused with nanoSiO₂ showed a compromised contractility, finding nanoSiO₂ accumulation (heart representation, left side). Once nanoSiO₂ internalizes into mitochondria, production of ROS is increased, compromising mitochondrial function. This leads to several oxidative damages, reducing the activity of the aconitase, and affecting the activity of key mitochondrial proteins such ANT through the oxidation of thiol groups. ANT oxidation promotes the mPTP formation, causing a decrease in mitochondrial membrane potential, which is the electrochemical force to synthetize ATP, compromising cellular viability. MitoTempo, a mitochondrial antioxidant agent, or CsA through delaying the formation of the mPTP, partially prevented these adverse effects of nanoSiO₂ exposure