Cardiotoxicity of chloroquine and hydroxychloroquine through mitochondrial pathway.


Journal

BMC pharmacology & toxicology
ISSN: 2050-6511
Titre abrégé: BMC Pharmacol Toxicol
Pays: England
ID NLM: 101590449

Informations de publication

Date de publication:
21 04 2023
Historique:
received: 07 01 2023
accepted: 27 03 2023
medline: 25 4 2023
pubmed: 22 4 2023
entrez: 21 04 2023
Statut: epublish

Résumé

Medical therapies can cause cardiotoxicity. Chloroquine (QC) and hydroxychloroquine (HQC) are drugs used in the treatment of malaria and skin and rheumatic disorders. These drugs were considered to help treatment of coronavirus disease (COVID-19) in 2019. Despite the low cost and availability of QC and HQC, reports indicate that this class of drugs can cause cardiotoxicity. The mechanism of this event is not well known, but evidence shows that QC and HQC can cause cardiotoxicity by affecting mitochondria and lysosomes. Therefore, our study was designed to investigate the effects of QC and HQC on heart mitochondria. In order to achieve this aim, mitochondrial function, reactive oxygen species (ROS) level, mitochondrial membrane disruption, and cytochrome c release in heart mitochondria were evaluated. Statistical significance was determined using the one-way and two-way analysis of variance (ANOVA) followed by post hoc Tukey to evaluate mitochondrial succinate dehydrogenase (SDH) activity and cytochrome c release, and Bonferroni test to evaluate the ROS level, mitochondrial membrane potential (MMP) collapse, and mitochondrial swelling. Based on ANOVA analysis (one-way), the results of mitochondrial SDH activity showed that the IC The results suggest that QC and HQC can cause cardiotoxicity which can lead to heart disorders through oxidative stress and disfunction of heart mitochondria.

Sections du résumé

BACKGROUND
Medical therapies can cause cardiotoxicity. Chloroquine (QC) and hydroxychloroquine (HQC) are drugs used in the treatment of malaria and skin and rheumatic disorders. These drugs were considered to help treatment of coronavirus disease (COVID-19) in 2019. Despite the low cost and availability of QC and HQC, reports indicate that this class of drugs can cause cardiotoxicity. The mechanism of this event is not well known, but evidence shows that QC and HQC can cause cardiotoxicity by affecting mitochondria and lysosomes.
METHODS
Therefore, our study was designed to investigate the effects of QC and HQC on heart mitochondria. In order to achieve this aim, mitochondrial function, reactive oxygen species (ROS) level, mitochondrial membrane disruption, and cytochrome c release in heart mitochondria were evaluated. Statistical significance was determined using the one-way and two-way analysis of variance (ANOVA) followed by post hoc Tukey to evaluate mitochondrial succinate dehydrogenase (SDH) activity and cytochrome c release, and Bonferroni test to evaluate the ROS level, mitochondrial membrane potential (MMP) collapse, and mitochondrial swelling.
RESULTS
Based on ANOVA analysis (one-way), the results of mitochondrial SDH activity showed that the IC
CONCLUSIONS
The results suggest that QC and HQC can cause cardiotoxicity which can lead to heart disorders through oxidative stress and disfunction of heart mitochondria.

Identifiants

pubmed: 37085872
doi: 10.1186/s40360-023-00666-x
pii: 10.1186/s40360-023-00666-x
pmc: PMC10119838
doi:

Substances chimiques

Hydroxychloroquine 4QWG6N8QKH
Chloroquine 886U3H6UFF
Reactive Oxygen Species 0
Cytochromes c 9007-43-6

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

26

Informations de copyright

© 2023. The Author(s).

Références

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Auteurs

Enayatollah Seydi (E)

Department of Occupational Health and Safety Engineering, School of Health, Alborz University of Medical Sciences, Karaj, Iran.
Research Center for Health, Safety and Environment, Alborz University of Medical Sciences, Karaj, Iran.

Mozhgan Karbalaei Hassani (MK)

Department of Toxicology and Pharmacology, School of Pharmacy, Shahid Beheshti University of Medical Sciences, Tehran, Iran.

Saghi Naderpour (S)

Faculty of Pharmacy, Eastern Mediterranean University, Famagusta, North Cyprus, Cyprus.

Abdollah Arjmand (A)

Department of Toxicology and Pharmacology, School of Pharmacy, Shahid Beheshti University of Medical Sciences, Tehran, Iran. a.arjmand@yahoo.com.

Jalal Pourahmad (J)

Department of Toxicology and Pharmacology, School of Pharmacy, Shahid Beheshti University of Medical Sciences, Tehran, Iran. j.pourahmadjaktaji@utoronto.ca.

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