Tissue examinations of glial tumors in the human brain revealed that therein lipid peroxidation could be induced by using bivalent iron salts, which is indicated by higher malonic dialdehyde levels. The authors have demonstrated that the glioma tissue levels of iron were statistically lower than those in the brain tissue. The induction in tumor tissue does not depend upon the degree of its malignancy, but it significantly differs from this parameter in the rabbit brain tissue. The induction of lipid peroxidation processes is accompanied by a lower cumulative antioxidative activity. The findings open new prospects for affecting tumor growth.
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Mol Med
January 2025
The First People's Hospital of Lin'an District, No. 360, Yikang Street, Jinnan Subdistrict, Lin'an District, Hangzhou, Zhejiang, 311300, China.
Background: Myocardial infarction (MI) remains a leading cause of mortality globally, often resulting in irreversible damage to cardiomyocytes. Ferroptosis, a recently identified form of regulated cell death driven by iron-dependent lipid peroxidation, has emerged as a significant contributor to post-MI cardiac injury. The endoplasmic reticulum (ER) stress response has been implicated in exacerbating ferroptosis.
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January 2025
Department of Pathology and Key Laboratory for Xinjiang Endemic and Ethnic Diseases, Shihezi University School of Medicine/The First Affiliated Hospital, Shihezi University, Shihezi 832002 China; Department of Pathology, Central People's Hospital of Zhanjiang and Zhanjiang Central Hospital, Guangdong Medical University, Zhanjiang 524000 Guangdong, China. Electronic address:
Background: In-stent restenosis (ISR) is one of the most significant complications following percutaneous coronary intervention (PCI) in patients with coronary artery disease (CAD). Ferroptosis is a novel cell death mode characterized by iron overload and lipid peroxidation. However, the role of ferroptosis in vascular smooth muscle cells (VSMCs) regulating neointimal formation during restenosis remains unclear.
View Article and Find Full Text PDFBiochimie
January 2025
Laboratory of Biochemistry and Molecular Neuropharmacology (LABIONEM), Graduate Program in Biochemistry and Bioprospecting (PPGBBio), Chemical, Pharmaceutical, and Food Sciences Center (CCQFA), Federal University of Pelotas (UFPel), 96010-900 RS, Brazil. Electronic address:
Oxidative stress arises from an imbalance between reactive species (RS) production and the antioxidant defense, increasing the brain susceptibility to neurodegenerative and psychiatric diseases. Besides, changes in the expression or activity of neurotransmitter metabolism enzymes, such as monoamine oxidases (MAO), are also associated with mental disorders, including depression. Considering this, antioxidant and MAO-A activity inhibitory potential of six 2,3-chalcogenodihydrobenzofurans (2,3-DHBF) was investigated through in vitro and in silico tests.
View Article and Find Full Text PDFFood Chem Toxicol
January 2025
Department of Pharmacology, Key Laboratory of Anti-Inflammatory and Immunopharmacology of Ministry of Education, Key Laboratory of Chinese Medicine Research and Development of State Administration of Traditional Chinese Medicine, Anhui Medical University, Hefei, Anhui, People's Republic of China. Electronic address:
Ischemic stroke is a very common brain disorder. This study aims to assess the neuroprotective effects of piceatannol (PCT) in preventing neuronal injury resulting from cerebral ischemia and reperfusion (I/R) in mice. Additionally, we investigated the underlying mechanisms through which PCT inhibits neuronal ferroptosis by modulating the USP14/GPX4 signaling axis.
View Article and Find Full Text PDFRedox Biol
January 2025
University of Chicago, Department of Molecular Genetics and Cell Biology, 929 E. 57th Street, Chicago, IL, 60637, USA. Electronic address:
During its catalytic cycle, the homodimeric ATPase topoisomerase II alpha (TOP2A) cleaves double stranded DNA and remains covalently bound to 5' ends via tyrosine phosphodiester bonds. After passing a second, intact duplex through, TOP2A rejoins the break and releases from the DNA. Thereby, TOP2A can relieve strain accumulated during transcription, replication and chromatin remodeling and disentangle sister chromatids for mitosis.
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