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 Q(10) (CoQ(10)), 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 CoQ(10) 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, CoQ(10) 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. CoQ(10) supplementation is postulated to counteract the adverse effects of amitriptyline treatment in psychiatric patients.
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Fluoxetine (as a fluorinated product) can induce hepatotoxicity, as a result to increased oxidative stress activity.
“In this way fluoxetine (as a fluorinated product) can induce hepatotoxicity, as a result to increased oxidative stress activity [266].”
From Oxidative Stress Implications in the Affective Disorders: Main Biomarkers, Animal Models Relevance, Genetic Perspectives, and Antioxidant Approaches (2016) · cites this paper as [266]
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“In this way fluoxetine (as a fluorinated product) can induce hepatotoxicity, as a result to increased oxidative stress activity [266].”
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- Authors
- Moreno-Fernández, A. M., Cordero, M. D., Garrido-Maraver, J., Alcocer-Gómez, E., Casas-Barquero, N., Carmona-López, M. I., Sánchez-Alcázar, J. A., & de Miguel, M.
- Affiliations
- Consejo Superior de Investigaciones Científicas (ES)
- Universidad de Sevilla (ES)
- Corresponding author
- Cordero, Mario D.
- Venue
- Journal of Psychiatric Research
- Publisher
- Elsevier BV
- Published
- 2012-03
- Volume
- 46
- Issue
- 3
- Pages
- 341-345
- ISSN
- 0022-3956 (ISSN-L)
- OpenAlex
- W1978539082
- Cited by
- 54
- References
- 31
- Citations by year
- 2026: 2 · 2025: 2 · 2024: 2 · 2023: 4 · 2022: 3 · 2021: 3 · 2020: 4 · 2019: 3 · 2018: 7 · 2017: 3 · 2016: 7 · 2015: 5 · 2014: 5 · 2013: 2 · 2012: 2
- FWCI
- 1.17
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Psychiatric Research (publishedVersion)
- PubMed (publishedVersion)
- DIGITAL.CSIC (Spanish National Research Council (CSIC)) (submittedVersion)
- Funders
- Universidad de Sevilla
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Coenzyme Q10 studies and effects
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Pharmacology › Treatment of Major Depression
- Keywords
- amitriptyline, coenzyme Q10 deficiency, oxidative stress, mitochondrial dysfunction, tricyclic antidepressants, depression, lipid peroxidation, ATP levels, mitochondrial mass, antidepressant side effects, coenzyme Q10 supplementation, psychiatric patients
- MeSH terms
- Adenosine Triphosphate, Administration, Oral, Adult, Amitriptyline, Antidepressive Agents, Tricyclic, Antioxidants, Avitaminosis, Depressive Disorder, Female, Humans, Male, Mitochondria, Ubiquinone, Biomarkers, Oxidative Stress, Dietary Supplements, Mitochondrial Diseases
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