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. 2020 Nov 30;9(12):1201. doi: 10.3390/antiox9121201

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© 2020 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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BPA effect on liver mitochondrial dysfunction and oxidative stress induced by HFD. (A) Mitochondrial state 3 and 4 respiration and (B) oxygen consumption linked to fatty acid oxidation were measured in the liver from all experimental groups using succinate or palmitoyl-carnitine as substrates, respectively. (C) The mitochondrial carnitine palmitoyl-transferase (CPT) activity in the liver of BPA-treated mice was determined. BPA worsening effect on HFD-induced (D) hepatic reactive oxygen species (ROS), and (E) malondialdehyde (MDA) levels was shown. Hepatic mitochondrial (F) superoxide dismutase (SOD) and (G) aconitase activity was spectrophotometrically measured. Data are presented as means ± SEM of all animals (n = 6 each group) (*** p < 0.001, and **** p < 0.0001 vs. STD; ^# p < 0.05, ^### p < 0.001, and ^#### p < 0.0001 vs. HFD).