Fluoxetine and the mitochondria: A review of the toxicological aspects

被引：67

作者：

de Oliveira, Marcos Roberto ^{[1
]}

机构：

[1] Fed Univ Mato Grosso UFMT, Dept Chem ICET, Av Fernando Correa da Costa, BR-78060900 Cuiaba, MT, Brazil

来源：

TOXICOLOGY LETTERS | 2016年 / 258卷

关键词：

Fluoxetine; Mitochondria; Respiratory chain; Reactive oxygen species; Apoptosis; NF-KAPPA-B; RAT-BRAIN MITOCHONDRIA; CELL-DEATH; OXIDATIVE STRESS; HYDROGEN-PEROXIDE; NEURONAL SURVIVAL; IN-VITRO; ANTIDEPRESSANT DRUGS; CARNOSIC ACID; BREAST-CANCER;

D O I：

10.1016/j.toxlet.2016.07.001

中图分类号：

R99 [毒物学（毒理学）];

学科分类号：

100405 ;

摘要：

Fluoxetine (a selective serotonin reuptake inhibitor (SSRI)) is used as an antidepressant by modulating the levels of serotonin in the synaptic cleft. Nevertheless, fluoxetine also induces undesirable effects, such as anxiety, sexual dysfunction, sleep disturbances, and gastrointestinal impairments. Fluoxetine has been viewed as an agent that may interfere with cell fate by triggering apoptosis. On the other hand, fluoxetine intake has been associated with increased cancer risk. Nonetheless, data remain contradictory and no conclusions were taken. Several studies demonstrated that fluoxetine interacts with mitochondria triggering apoptosis and/or altering mitochondrial function by modulating the activity of respiratory chain components and enzymes of the Krebs cycle. Furthermore, fluoxetine affects mitochondria-related redox parameters in different experimental models. In this review, data demonstrating the effects of fluoxetine upon mammalian mitochondria are described and discussed, as well as several unsolved questions in this field of research are addressed. A separate section deals with future needs regarding the research involving the impact of fluoxetine treatment upon mitochondria and mitochondria-related signaling. (C) 2016 Elsevier Ireland Ltd. All rights reserved.

引用

页码：185 / 191

页数：7

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