Chrysin ameliorates aluminum phosphide-induced oxidative stress and mitochondrial damages in rat cardiomyocytes and isolated mitochondria.
Aluminum Compounds
/ toxicity
Animals
Cardiotoxicity
Cells, Cultured
Flavonoids
/ pharmacology
Glutathione
/ metabolism
Humans
Lipid Peroxidation
/ drug effects
Lysosomes
/ metabolism
Male
Membrane Potential, Mitochondrial
/ drug effects
Mitochondria, Heart
/ drug effects
Mitochondrial Swelling
/ drug effects
Myocytes, Cardiac
/ drug effects
Oxidative Stress
/ drug effects
Phosphines
/ toxicity
Protective Agents
/ pharmacology
Rats
Rats, Wistar
Reactive Oxygen Species
/ metabolism
aluminum phosphide
cardiomyocytes
cardiotoxicity
chrysin
mitochondria
Journal
Environmental toxicology
ISSN: 1522-7278
Titre abrégé: Environ Toxicol
Pays: United States
ID NLM: 100885357
Informations de publication
Date de publication:
Oct 2020
Oct 2020
Historique:
received:
09
01
2020
revised:
23
04
2020
accepted:
06
05
2020
pubmed:
21
5
2020
medline:
9
10
2020
entrez:
21
5
2020
Statut:
ppublish
Résumé
Apart from the anticancer, antioxidant, anti-inflammatory effects, and inhibition of aromatase, chrysin is involved in the protection of cardiovascular disorders. Cardiovascular complications are the main cause of death induced by aluminum phosphide (AlP) which is related to oxidative stress and mitochondrial damages. For this purpose, we investigated the effect of chrysin as an antioxidant and mitochondrial protective agent against AlP-induced toxicity in isolated cardiomyocytes and mitochondria obtained from rat heart ventricular. Using by biochemical and flow cytometry, cell viability, reactive oxygen species (ROS) formation, mitochondria membrane potential (MMP), lysosomal membrane integrity, malondialdehyde (MDA) content, and glutathione (GSH) and oxidized glutathione (GSSG) content were measured in isolated cardiomyocytes. Also, mitochondrial toxicity parameters such as mitochondrial NADH/succinate dehydrogenase activity, mitochondrial swelling, ROS formation, MMP collapse, and lipid peroxidation were analyzed in isolated mitochondria. Our results showed that the administration of chrysin (up to 10 μM) efficiently decreased (P < 0.05) cytotoxicity, oxidative, lysosomal, and mitochondrial damages induced by AlP, in isolated cardiomyocytes. Also, our finding in isolated mitochondria showed that chrysin (up to 10 μM) significantly (P < 0.05) decreased AlP-induced mitochondrial toxicity. These findings demonstrated that chrysin as an antioxidant and mitochondrial protective agent exert protective effect in wild-type cardiomyocyte treated with AlP. It was concluded that chrysin significantly reduced the toxicity of AlP in isolated cardiomyocytes and mitochondria. Due to the very low toxicity of chrysin for humans, it could be a promising agent in treatment of AlP poisoning.
Substances chimiques
Aluminum Compounds
0
Flavonoids
0
Phosphines
0
Protective Agents
0
Reactive Oxygen Species
0
chrysin
3CN01F5ZJ5
aluminum phosphide
E23DR6L59S
Glutathione
GAN16C9B8O
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
1114-1124Subventions
Organisme : Ardabil University of Medical Sciences
ID : IR.ARUMS.REC.1398.273
Organisme : Ardabil University of Medical Sciences
ID : IR.ARUMS.REC.1398.167
Informations de copyright
© 2020 Wiley Periodicals LLC.
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