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Updated: Dec 28, 2025

Mitochondrial Respiration Quantification in Yeast Whole Cells
Published on: November 8, 2024
Protective effects of quercetin against oxidative stress induced by bisphenol-A in rat cardiac mitochondria
Atefeh Raesi Vanani1,2, Masoud Mahdavinia1,2, Maryam Shirani3
1Toxicology Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
Abstract:
Research has shown a relationship between the exposures to a chemical agent called bisphenol-A (BPA), which is extensively used in the production of polycarbonate plastics and the incidence of cardiovascular diseases. This association is most likely caused by the BPA's ability to disrupt multiple cardiac mechanisms, including mitochondrial functions. Therefore, this study aimed to explore the ability of quercetin (QUER) to limit the cardiotoxic effect of BPA in the rat's cardiac mitochondria. The experiment was carried out on 32 male Wistar rats, which were randomly assigned to four groups. The negative control group received olive oil; the positive control group received olive oil plus BPA (250 mg/kg); the third group received olive oil, BPA, and QUER (75 mg/kg); and the fourth group received olive oil and QUER, all orally for 14 days. The rats were slaughtered 24 h after the last treatment. The measured parameters included creatine kinase-MB (CK-MB) and lactate dehydrogenase (LDH) as the biomarkers of cardiotoxicity, triglyceride (TG), total cholesterol (TC), and low-density and high-density lipoprotein cholesterol (LDL-C and HDL-C) as the measures of dyslipidemia, glutathione (GSH) content, catalase activity (CAT), reactive oxygen species (ROS), lipid peroxidation (LPO), and the level of damage to the mitochondrial membranes as the indicators of the impact of QUER on the BPA cardiotoxic effect. Finally, the rats treated with QUER showed better results in terms of serum CK-MB, serum LDH, serum lipid profile, GSH level, CAT activity, mitochondrial membrane potential (ΔΨm), LPO, and ROS. According to the results, QUER could be used as a protective agent against BPA-induced mitochondrial toxicity.
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