ArticleFrontiers in pharmacology2021
Antioxidant Potential and Inhibition of Mitochondrial Permeability Transition Pore by Myricetin Reduces Aluminium Phosphide-Induced Cytotoxicity and Mitochondrial Impairments.
Article in Frontiers in pharmacology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 28 citations in OpenAlex.
- Myricetin alleviates testosterone-induced benign prostatic hyperplasia by attenuating inflammation, oxidative stress, apoptosis and androgen signaling.Scientific reports · 2026Article
- Mitochondrial CaJournal of cellular physiology · 2025Review
- Comprehensive Physiological and Transcriptomic Profiling of Triploid Pacific Oysters (Biology · 2025Article
- Magnetic molecularly imprinted polymers for efficient solid-phase extraction and HPLC analysis of myricetin in pomegranate pomace.RSC advances · 2025Article
- Unlocking the Pharmacological Potential of Myricetin Against Various Pathogenesis.International journal of molecular sciences · 2025Review
- Black soldier fly larvae oil can partially replace fish oil in the diet of the juvenile mud crab (Animal nutrition (Zhongguo xu mu shou yi xue hui) · 2025Article
- Evaluation of the Protective Effects of Lugol's Solution in Rats Poisoned with Aluminum Phosphide (Rice Tablets).Cardiovascular toxicology · 2024Article
- Mitotherapy with Fresh Isolated Cardiac Mitochondria Via Injection Into Blood Reduces Aluminum Phosphide-Induced Mortality and Protects Cardiac Tissue Against Oxidative Stress and Mitochondrial Damages.Cardiovascular toxicology · 2024Article
- Shock and modified shock indices in predicting poisoning severity and outcomes in acute aluminum phosphide poisoned patients.Toxicology research · 2024Article
- Newly Synthesized Creatine Derivatives as Potential Neuroprotective and Antioxidant Agents on In Vitro Models of Parkinson's Disease.Life (Basel, Switzerland) · 2023Article
- Recent studies on myricetin and its biological and pharmacological activities.EXCLI journal · 2023Article
- The Neuroprotective Potentiality of Flavonoids on Alzheimer's Disease.International journal of molecular sciences · 2022Review
- From Myricetin to the Discovery of Novel Natural Human ENPP1 Inhibitors: A Virtual Screening, Molecular Docking, Molecular Dynamics Simulation, and MM/GBSA Study.Molecules (Basel, Switzerland) · 2022Article
- Myricetin (3,3',4',5,5',7-Hexahydroxyflavone) Prevents 5-Fluorouracil-Induced Cardiotoxicity.ACS omega · 2022Article
- Quercetin Protected from Aluminum Phosphide-induced Acute and Subacute Cardio- and Hepatotoxicity in Rats.Current pharmaceutical design · 2022Article
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Authors and funding
3 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Oxidative stress and mitochondrial dysfunction are involved in the mechanisms of cardiac toxicity induced by aluminum phosphide (AlP). AlP-induced cardiotoxicity leads to cardiomyocyte death, cardiomyopathy, cardiac dysfunction, and eventually severe heart failure and death. Importantly, protecting cardiomyocytes from death resulting from AlP is vital for improving survival. It has been reported that flavonoids such as myricetin (Myr) act as modifiers of mitochondrial function and prevent mitochondrial damage resulting from many insults and subsequent cell dysfunction. In this study, the ameliorative effect of Myr, as an important antioxidant and mitochondrial protective agent, was investigated in cardiomyocytes and mitochondria isolated from rat heart against AlP-induced toxicity, oxidative stress, and mitochondrial dysfunction. Treatment of AlP (20 μg/ml) significantly increased cytotoxicity; reduced glutathione (GSH) depletion, cellular reactive oxygen species (ROS) formation, malondialdehyde (MDA) level, ATP depletion, caspase-3 activation, mitochondrial membrane potential (ΔΨm) collapse, and lysosomal dysfunction; and decreased the activities of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) in intact cardiomyocytes. Also, treatment of AlP (20 μg/ml) significantly increased mitochondrial dysfunction and swelling in isolated mitochondria. Myr (80 µM) appeared to ameliorate AlP-induced cytotoxicity in isolated cardiomyocytes; significantly lessened the AlP-stimulated intracellular ROS and MDA production and depletion of GSH; and increased the activities of SOD, CAT, and GSH-Px. Furthermore, Myr (40 and 80 µM) lowered AlP-induced lysosomal/mitochondrial dysfunction, ATP depletion, and caspase-3 activation. In the light of these findings, we concluded that Myr through antioxidant potential and inhibition of mitochondrial permeability transition (MPT) pore exerted an ameliorative role in AlP-induced toxicity in isolated cardiomyocytes and mitochondria, and it would be valuable to examine its
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