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Additionally, thyroid hormone increased the quality of mitochondria by inducing PGC-1 and ULK1 in HepG2 cells and mouse liver tissues, which suggested the potential use of ERR agonists in metabolic illnesses through enhancing mitochondrial function [211]

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The net agonist-induced preference or aversion is critically dependent on dose

Pawlowska E, Szczepanska J, Blasiak J

Summarizing the available data from animal studies, we can conclude that oxidative damage of the brain during treatment with typical antipsychotics is due to the following mechanisms: A significant decrease in the activity of Mn-SOD, Cu,Zn-SOD, and catalase Increased lipid peroxidation of membranes Reduction of NO concentration [345] Increased production of superoxide and H 2 O 2 [345] Human studies also indicate that antipsychotics contribute to oxidative stress [346]

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