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Direct scavenging of free radicals (especially ROS), inhibition of ROS manufacturing enzymes, and preservation of mitochondrial integrity and function affect redox signaling by activating nuclear factor erythroid-derived 2-like 2 (Nrf2) and peroxisome proliferator-activated receptor alpha (PPAR), and the synthesis of heat shock proteins (HSPs), thioredoxins, sirtuins, and other antioxidant molecules are pathways through which L-carnitine and its derivatives modulate oxidative stress conditions [14, 38]

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Oxidative stress assessment by immuno-fluorescence ROS levels were also assessed using the dihydroethidium (DHE) probe, according to previously published protocols [28, 29]