Reserpine as an uncoupler of oxidative phosphorylation and the relevance to its psychoactive properties
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2013, Neuroscience and Biobehavioral ReviewsCitation Excerpt :More specifically, antidepressants (sertraline, desipramine, amitriptyline, imipramine, citalopram, mirtazapine and fluoxetine) as well as mood stabilizers (valproate and olanzapine) may act generally as inhibitors of mitochondrial electron transport chain (e.g. Burkhardt et al., 1993; Daley et al., 2005; Finsterer, 2006; Hroudova and Fisar, 2011; Li et al., 2012; Maurer and Moller, 1997; Neustadt and Pieczenik, 2008). Furthermore, tricyclic antidepressants, like imipramine, fluoxetine, and chlorimipramine exhibit some characteristics of classic uncouplers of oxidative phosphorylation, as they released respiratory control, hindered ATP synthesis and enhanced ATPase activity (Hroudova and Fisar, 2011; Weinbach et al., 1983). Furthermore, in vivo studies demonstrated that nefazodone-induced hepatotoxicity attributed to inhibition of mitochondrial respiratory complexes I and IV and depolarization of the mitochondrial membrane (Dykens et al., 2008).
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2007, Chemico-Biological InteractionsCitation Excerpt :This usually results in diminished cellular ATP production [39]. Reserpine, has been shown to uncouple oxidative phosphorylation in mitochondria [40] and has been reported to deplete ATP and decrease ADP/O ratio [41]. Gastric mucosal injury also results in ATP depletion in gastric mucosa [42] which concurs with the present study that ibuprofen and reserpine caused mitochondrial ATP depletion leading to mitochondrial dysfunction.
Effect of catecholamine depletion on oxidative energy metabolism in rat liver, brain and heart mitochondria; use of reserpine
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