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Chrysin ameliorates aluminum p hosphide‐induced oxidative stress and mitochondrial damages in rat cardiomyocytes and isolated mitochondria
Environmental Toxicology ( IF 4.5 ) Pub Date : 2020-05-20 , DOI: 10.1002/tox.22947
Saleh Khezri 1 , Towhid Sabzalipour 1 , Asal Jahedsani 1 , Sepideh Azizian 1 , Saman Atashbar 1 , Ahmad Salimi 1
Affiliation  

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.

中文翻译:

白杨素改善磷化铝诱导的大鼠心肌细胞和分离线粒体中的氧化应激和线粒体损伤

除了抗癌、抗氧化、抗炎作用和抑制芳香酶外,白杨素还参与心血管疾病的保护。心血管并发症是磷化铝(AlP)致死的主要原因,其与氧化应激和线粒体损伤有关。为此,我们研究了白杨素作为抗氧化剂和线粒体保护剂对从大鼠心室获得的离体心肌细胞和线粒体中 AlP 诱导的毒性的影响。使用生化和流式细胞术,测量细胞活力、活性氧 (ROS) 形成、线粒体膜电位 (MMP)、溶酶体膜完整性、丙二醛 (MDA) 含量以及谷胱甘肽 (GSH) 和氧化型谷胱甘肽 (GSSG) 含量分离的心肌细胞。还,在分离的线粒体中分析了线粒体毒性参数,例如线粒体 NADH/琥珀酸脱氢酶活性、线粒体肿胀、ROS 形成、MMP 崩溃和脂质过氧化。我们的结果表明,白杨素(高达 10 μM)的施用有效地降低了(P < 0.05)AlP 诱导的分离心肌细胞中的细胞毒性、氧化性、溶酶体和线粒体损伤。此外,我们在分离线粒体中的发现表明白杨素(高达 10 μM)显着(P < 0.05)降低了 AlP 诱导的线粒体毒性。这些发现表明,白杨素作为抗氧化剂和线粒体保护剂对用 AlP 处理的野生型心肌细胞发挥保护作用。结论是白杨素显着降低了分离的心肌细胞和线粒体中AlP的毒性。
更新日期:2020-05-20
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