Radiobiological damage is principally triggered by an initial cation and a secondary electron (SE). We address the fundamental questions: What lesions are first produced in DNA by this cation or nonionizing SE? What are their relative contributions to isolated and potentially lethal cluster lesions? Five monolayer films of dry plasmid DNA deposited on graphite or tantalum substrates are bombarded by 0.1-100 eV electrons in a vacuum. From measurements of the current transmitted through the films, 3.5 and 4.5 cations per incident 60 and 100 eV electrons, respectively, are estimated to be produced and stabilized within DNA. Damage analysis at 6, 10, 20, 30, 60, and 100 eV indicates that essentially all lesions, but preferentially cluster damages, are produced by non-ionizing or weakly ionizing electrons of energies below 12 eV. Most of these lesions are induced within femtosecond times, via transient anions and electron transfer within DNA, with little contributions from the numerous cations.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1021/acs.jpclett.0c03341 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Recent advances in biomarkers for senescence: Bridging basic research to clinic.
Geriatr Gerontol Int
January 2025
Department of Advanced Senotherapeutics and Department of Cardiovascular Biology and Medicine, Juntendo University Graduate School of Medicine, Tokyo, Japan.
In this review, we review the current status of biomarkers for aging and possible perspectives on anti-aging or rejuvenation from the standpoint of biomarkers. Aging is observed in all cells and organs, and we focused on research into senescence in the skin, musculoskeletal system, immune system, and cardiovascular system. Commonly used biomarkers include SA-βgal, cell-cycle markers, senescence-associated secretory phenotype (SASP) factors, damage-associated molecular patterns (DAMPs), and DNA-damage-related markers.
View Article and Find Full Text PDFCYP3A5 promotes glioblastoma stemness and chemoresistance through fine-tuning NAD/NADH ratio.
J Exp Clin Cancer Res
January 2025
School of Medicine, Chinese PLA General Hospital, Nankai University, Beijing, China.
Background: Glioblastoma multiforme (GBM) exhibits a cellular hierarchy with a subpopulation of stem-like cells known as glioblastoma stem cells (GSCs) that drive tumor growth and contribute to treatment resistance. NAD(H) emerges as a crucial factor influencing GSC maintenance through its involvement in diverse biological processes, including mitochondrial fitness and DNA damage repair. However, how GSCs leverage metabolic adaptation to obtain survival advantage remains elusive.
View Article and Find Full Text PDFATM and IRAK1 orchestrate two distinct mechanisms of NF-κB activation in response to DNA damage.
Nat Struct Mol Biol
January 2025
Department of Biological Chemistry, School of Medicine, University of California Irvine, Irvine, CA, USA.
DNA damage in cells induces the expression of inflammatory genes. However, the mechanism by which cells initiate an innate immune response in the presence of DNA lesions blocking transcription remains unknown. Here we find that genotoxic stresses lead to an acute activation of the transcription factor NF-κB through two distinct pathways, each triggered by different types of DNA lesions and coordinated by either ataxia-telangiectasia mutated (ATM) or IRAK1 kinases.
View Article and Find Full Text PDFNUFIP1 integrates amino acid sensing and DNA damage response to maintain the intestinal homeostasis.
Nat Metab
January 2025
Fudan University Shanghai Cancer Center and Institutes of Biomedical Sciences; School of Basic Medical Sciences, Cancer Institutes; Key Laboratory of Breast Cancer in Shanghai; Shanghai Key Laboratory of Radiation Oncology; the Shanghai Key Laboratory of Medical Epigenetics, State Key Laboratory of Medical Neurobiology, Shanghai Medical College, Fudan University, Shanghai, China.
Nutrient availability strongly affects intestinal homeostasis. Here, we report that low-protein (LP) diets decrease amino acids levels, impair the DNA damage response (DDR), cause DNA damage and exacerbate inflammation in intestinal tissues of male mice with inflammatory bowel disease (IBD). Intriguingly, loss of nuclear fragile X mental retardation-interacting protein 1 (NUFIP1) contributes to the amino acid deficiency-induced impairment of the DDR in vivo and in vitro and induces necroptosis-related spontaneous enteritis.
View Article and Find Full Text PDFEndothelial-Ercc1 DNA repair deficiency provokes blood-brain barrier dysfunction.
Cell Death Dis
January 2025
Amsterdam UMC location Vrije Universiteit Amsterdam, Department of Molecular Cell Biology and Immunology, De Boelelaan 1117, 1081 HV, Amsterdam, The Netherlands.
Aging of the brain vasculature plays a key role in the development of neurovascular and neurodegenerative diseases, thereby contributing to cognitive impairment. Among other factors, DNA damage strongly promotes cellular aging, however, the role of genomic instability in brain endothelial cells (EC) and its potential effect on brain homeostasis is still largely unclear. We here investigated how endothelial aging impacts blood-brain barrier (BBB) function by using excision repair cross complementation group 1 (ERCC1)-deficient human brain ECs and an EC-specific Ercc1 knock out (EC-KO) mouse model.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!