Oral treatment with amitriptyline induces coenzyme Q deficiency and oxidative stress in psychiatric patients

Abstract Amitriptyline is a commonly prescribed tricyclic antidepressant, which has been shown to impair mitochondrial function and increase oxidative stress in a variety of in vitro assays. Coenzyme Q10 (CoQ10 ), an essential component of the mitochondrial respiratory chain and a potent antioxidant...

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Published in:Journal of psychiatric research Vol. 46; no. 3; pp. 341 - 345
Main Authors: Moreno-Fernández, Ana M, Cordero, Mario D, Garrido-Maraver, Juan, Alcocer-Gómez, Elísabet, Casas-Barquero, Nieves, Carmona-López, María I, Sánchez-Alcázar, José Antonio, de Miguel, Manuel
Format: Journal Article
Language:English
Published: Kidlington Elsevier Ltd 01-03-2012
Elsevier
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Summary:Abstract Amitriptyline is a commonly prescribed tricyclic antidepressant, which has been shown to impair mitochondrial function and increase oxidative stress in a variety of in vitro assays. Coenzyme Q10 (CoQ10 ), an essential component of the mitochondrial respiratory chain and a potent antioxidant, has been proposed as a mitochondrial dysfunction marker. In order to evaluate the putative mitochondrial toxicity of amitriptyline, we have analyzed CoQ10 and ATP levels, oxidative damage and mitochondrial mass in peripheral blood cells from control healthy volunteers and psychiatric patients with depressive episodes treated or non-treated with amitriptyline. In patients not following amitriptyline treatment, CoQ10 and ATP levels and mitochondrial mass were reduced when compared to normal individuals while lipid peroxidation was clearly increased. All these alterations were aggravated in patients following oral amitriptyline therapy. These results suggest that mitochondrial dysfunction could be involved in the pathophysiology of depression and may be worsened by amitriptyline treatment. CoQ10 supplementation is postulated to counteract the adverse effects of amitriptyline treatment in psychiatric patients.
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ISSN:0022-3956
1879-1379
DOI:10.1016/j.jpsychires.2011.11.002