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Related Experiment Video

Updated: May 24, 2026

Using Live Cell STED Imaging to Visualize Mitochondrial Inner Membrane Ultrastructure in Neuronal Cell Models

Using Live Cell STED Imaging to Visualize Mitochondrial Inner Membrane Ultrastructure in Neuronal Cell Models

Published on: June 30, 2023

Mitochondrial dysfunction induced by sertraline, an antidepressant agent.

Yan Li¹, Letha Couch, Masahiro Higuchi

¹Division of Genetic and Molecular Toxicology, National Center for Toxicological Research/U.S. FDA, Jefferson, Arkansas 72079, USA.

Toxicological Sciences : an Official Journal of the Society of Toxicology

|March 6, 2012

Summary

Sertraline, an antidepressant, may cause liver injury by impairing mitochondria. This study found sertraline disrupts cellular energy production and triggers cell damage, suggesting mitochondrial dysfunction as a key mechanism in sertraline hepatotoxicity.

Related Experiment Videos

Last Updated: May 24, 2026

Using Live Cell STED Imaging to Visualize Mitochondrial Inner Membrane Ultrastructure in Neuronal Cell Models

Using Live Cell STED Imaging to Visualize Mitochondrial Inner Membrane Ultrastructure in Neuronal Cell Models

Published on: June 30, 2023

Area of Science:

Biochemistry
Hepatology
Pharmacology

Background:

Sertraline, a selective serotonin reuptake inhibitor (SSRI), is widely used for depression.
While generally safe, sertraline has been linked to rare cases of liver injury (hepatotoxicity).
The precise mechanism underlying sertraline-induced hepatotoxicity remains unknown.

Purpose of the Study:

To investigate the role of mitochondrial dysfunction in sertraline-associated liver injury.
To elucidate the molecular mechanisms by which sertraline may induce hepatotoxicity.

Main Methods:

Isolated rat liver mitochondria were used to assess oxidative phosphorylation and complex activities.
Mitochondrial permeability transition (MPT) was induced and inhibited using specific agents.
Primary rat hepatocytes were treated with sertraline to measure adenosine triphosphate (ATP) levels and lactate dehydrogenase (LDH) leakage.

Main Results:

Sertraline uncoupled mitochondrial oxidative phosphorylation and inhibited complexes I and V.
Sertraline induced calcium-mediated MPT, mediated by the adenine nucleotide translocator (ANT).
In hepatocytes, sertraline depleted ATP and increased LDH leakage, effects attenuated by an MPT inhibitor.

Conclusions:

Mitochondrial dysfunction, including impaired oxidative phosphorylation and MPT induction, plays a significant role in sertraline-induced liver injury.
Sertraline's hepatotoxicity may be mediated through the disruption of mitochondrial function and cellular energy homeostasis.
These findings provide a potential mechanism for sertraline-associated hepatotoxicity.