This introductory article should be viewed as a prologue to the Free Radical Biology & Medicine Special Issue devoted to the important topic of Oxidatively Damaged DNA and its Repair. This special issue is dedicated to Professor Tomas Lindahl, co-winner of the 2015 Nobel Prize in Chemistry for his seminal discoveries in the area repair of oxidatively damaged DNA. In the past several years it has become abundantly clear that DNA oxidation is a major consequence of life in an oxygen-rich environment. Concomitantly, survival in the presence of oxygen, with the constant threat of deleterious DNA mutations and deletions, has largely been made possible through the evolution of a vast array of DNA repair enzymes. The articles in this Oxidatively Damaged DNA & Repair special issue detail the reactions by which intracellular DNA is oxidatively damaged, and the enzymatic reactions and pathways by which living organisms survive such assaults by repair processes.
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http://dx.doi.org/10.1016/j.freeradbiomed.2017.03.030 | DOI Listing |
Proc Natl Acad Sci U S A
February 2025
Cardiovascular Research Institute, University of California San Francisco, San Francisco, CA 94158.
The ε4 variant of human apolipoprotein E () is a key genetic risk factor for neurodegeneration in Alzheimer's disease and elevated all-cause mortality in humans. Understanding the factors and mechanisms that can mitigate the harmful effects of has significant implications. In this study, we find that inactivating the VHL-1 (Von Hippel-Lindau) protein can suppress mortality, neural and behavioral pathologies caused by transgenic human in .
View Article and Find Full Text PDFProc Natl Acad Sci U S A
February 2025
Center for Medical Research and Innovation, Shanghai Pudong Hospital, Institutes of Biomedical Sciences, Chinese Academy of Medical Sciences (RU069), Medical College of Fudan University, Shanghai 201399, China.
Ten-eleven translocation (TET) enzymes oxidize 5-methylcytosine (mC) in DNA, contributing to the regulation of gene transcription. Diverse mutations of TET2 are frequently found in various blood cancers, yet the full scope of their functional consequences has been unexplored. Here, we report that a subset of TET2 mutations identified in leukemia patients alter the substrate specificity of TET2 from acting on mC to thymine.
View Article and Find Full Text PDFToxicol Ind Health
January 2025
Department of of Toxicology, Faculty of Pharmacy, Istanbul Okan University, Istanbul, Turkey.
Di-2-(ethylhexyl)phthalate (DEHP) is a phthalate derivative used extensively in a wide range of materials, such as medical devices, toys, cosmetics, and personal care products. Many mechanisms, including epigenetics, may be involved in the effects of phthalates on brain development. In this study, Sprague-Dawley male rats were obtained 21-23 days after their birth (post-weaning) and were exposed to DEHP during the prepubertal period with low-dose DEHP (DEHP-L, 30 mg/kg/day) and high-dose DEHP (DEHP-H, 60 mg/kg/day, 37 days) until the end of adolescence (PND 60).
View Article and Find Full Text PDFEnviron Toxicol
January 2025
Cardiovascular Center, College of Medicine, University of Cincinnati, Cincinnati, Ohio, USA.
The cardiovascular risks linked to PM include calcification in both vasculature and myocardial tissues, leading to structural changes and functional decline. Through the selection of a clinically proven endogenous agent, sodium thiosulfate (STS), capable of addressing PM related cardiac abnormalities, we not only address the absence of effective solutions to mitigate PM toxicity, but also provide evidence for the repurposing potential of STS in ameliorating PM induced cardiac damage. Female Wistar rats were exposed to PM (250 μg/m) for 3 h daily for 21 days.
View Article and Find Full Text PDFJ Cachexia Sarcopenia Muscle
February 2025
Department of Bioactive Material Sciences, Research Center of Bioactive Materials, Jeonbuk National University, Jeonju, Republic of Korea.
Background: The cellular prion protein (PrP), a glycoprotein encoded by the PRNP gene, is known to modulate muscle mass and exercise capacity. However, the role of PrP in the maintenance and regeneration of skeletal muscle during ageing remains unclear.
Methods: This study investigated the change in PrP expression during muscle formation using C2C12 cells and evaluated muscle function in Prnp wild-type (WT) and knock-out (KO) mice at different ages (1, 9 and 15 months).
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