Recent studies have demonstrated that bisphenol A (BPA) has an adverse or toxic effect on the kidney. This study was designed to evaluate the ability of quercetin (QUER) to prevent BPA-induced mitochondrial dysfunction. Thirty-two healthy adult male Wistar rats were randomly divided into four groups, as follows: control group (olive oil), BPA group (250 mg/kg), BPA þ QUER group (250 mg/kg + 75 mg/kg), and QUER group (75 mg/kg). All treatments were orally administered for 14 days. Kidney mitochondria were isolated by administration of the different centrifugation method. Uric acid and creatinine were considered to be biomarkers of nephrotoxicity. The ameliorative effects of QUER on BPA toxicity were evaluated by determining the glutathione (GSH) content, CAT, the damage to the mitochondrial membrane, the reactive oxygen species (ROS), and lipid peroxidation (LPO). Administration of BPA significantly decreased kidney weight. In the kidney, BPA can deplete GSH content and CAT activity, increase the mitochondrial ROS formation, and enhances LPO and mitochondrial membrane damage. The pretreatment of mitochondria with QUER has the ability to reduce the toxic effects of BPA in isolated mitochondria. These findings suggest a potential role for QUER in protecting mitochondria from oxidative damage in kidney tissue.
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http://dx.doi.org/10.1007/s11356-018-04119-5 | DOI Listing |
ACS Nano
January 2025
National Synchrotron Radiation Laboratory, University of Science and Technology of China, Hefei 230026, China.
Metal ions are indispensable to life, as they can serve as essential enzyme cofactors to drive fundamental biochemical reactions, yet paradoxically, excess is highly toxic. Higher-order cells have evolved functionally distinct organelles that separate and coordinate sophisticated biochemical processes to maintain cellular homeostasis upon metal ion stimuli. Here, we uncover the remodeling of subcellular architecture and organellar interactome in yeast initiated by several metal ion stimulations, relying on near-native three-dimensional imaging, cryo-soft X-ray tomography.
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Department of Cardiology, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, China.
Mitochondrial transplantation (MT) is a promising therapeutic strategy that involves introducing healthy mitochondria into damaged tissues to restore cellular function. This approach has shown promise in treating cardiac diseases, such as ischemia-reperfusion injury, myocardial infarction, and heart failure, where mitochondrial dysfunction plays a crucial role. Transplanting healthy mitochondria into affected cardiac tissue has resulted in improved cardiac function, reduced infract size, and enhanced cell survival in preclinical studies.
View Article and Find Full Text PDFJ Inflamm Res
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State Key Laboratory of Oral & Maxillofacial Reconstruction and Regeneration, Key Laboratory of Oral Biomedicine Ministry of Education, Hubei Key Laboratory of Stomatology, School & Hospital of Stomatology, Wuhan University, Wuhan, People's Republic of China.
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View Article and Find Full Text PDFSci Rep
January 2025
Laboratory for Critical Care Physiology, Feinstein Institutes for Medical Research, Northwell Health, Manhasset, NY, USA.
Mitochondrial transplantation (MTx) offers a promising therapeutic approach to mitigate mitochondrial dysfunction in conditions such as ischemia-reperfusion (IR) injury. The quality and viability of donor mitochondria are critical to MTx success, necessitating the optimization of isolation protocols. This study aimed to assess a rapid mitochondrial isolation method, examine the relationship between mitochondrial size and membrane potential, and evaluate the potential benefits of Poloxamer 188 (P-188) in improving mitochondrial quality during the isolation process.
View Article and Find Full Text PDFChemistry
January 2025
ETH Zürich, Institute of Pharmaceutical Sciences, Höneggerberg, HCI H427, Vladimir Prelog Weg 4, 8093, Zürich, SWITZERLAND.
ATP synthase dysregulation has been implicated in many diseases, including cancer and neurodegenerative diseases. Whilst ATP synthase-targeting compounds have been reported, most are large or polar compounds and lack appropriate properties for a CNS drug. We designed, synthesised, and evaluated a novel series of ATP synthase targeting compounds, resulting in a 1,3,4-oxadiazin-5-one scaffold with improved physiochemical properties.
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