ArticleInternational journal of molecular sciences2023
Comet Assay Profiling of FLASH-Induced Damage: Mechanistic Insights into the Effects of FLASH Irradiation.
Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 19 citations in OpenAlex.
- FLASH radiotherapy enables dose escalation resulting in improved survival in an orthotopic muscle-invasive bladder cancer mouse model.The British journal of radiology · 2026Article
- DNA damage and cell death induced by exposure to ultra-high dose rate low-dose pulsed X-rays emitted from a kilojoule plasma focus device.Biological research · 2026Article
- Biological effects of conventional and ultra high dose rate radiation in human cells.Scientific reports · 2026Article
- In vitro oxygen concentration alters reactive oxygen species yields with minor plasmid DNA damage change at ultra-high-dose rate.The British journal of radiology · 2026Article
- Cytogenetic Effects of Conventional and Ultra High Dose Rates of Radiation in Human Lymphocytes: Comparative Analysis in Metaphase Chromosomes and G2-PCCs.Disaster medicine and public health preparedness · 2025Article
- Factors Influencing the Biological Effects of FLASH Irradiation.Antioxidants (Basel, Switzerland) · 2025Review
- FLASH-induced DNA damage reduction measured in vitro correlates with effective oxygen depletion determined in silico: further support for oxygen depletion contributing to FLASH's reduced damage burden in vitro.The British journal of radiology · 2025Article
- Mathematical modeling in radiotherapy for cancer: a comprehensive narrative review.Radiation oncology (London, England) · 2025Review
- Effect of Ultrahigh Dose Rate on Biomolecular Radiation Damage.Radiation research · 2024Article
- FLASH Radiotherapy: Expectations, Challenges, and Current Knowledge.International journal of molecular sciences · 2024Review
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Numerous studies have demonstrated the normal tissue-sparing effects of ultra-high dose rate 'FLASH' irradiation in vivo, with an associated reduction in damage burden being reported in vitro. Towards this, two key radiochemical mechanisms have been proposed: radical-radical recombination (RRR) and transient oxygen depletion (TOD), with both being proposed to lead to reduced levels of induced damage. Previously, we reported that FLASH induces lower levels of DNA strand break damage in whole-blood peripheral blood lymphocytes (WB-PBL) ex vivo, but our study failed to distinguish the mechanism(s) involved. A potential outcome of RRR is the formation of crosslink damage (particularly, if any organic radicals recombine), whilst a possible outcome of TOD is a more anoxic profile of induced damage resulting from FLASH. Therefore, the aim of the current study was to profile FLASH-induced damage via the Comet assay, assessing any DNA crosslink formation as a putative marker of RRR and/or anoxic DNA damage formation as an indicative marker of TOD, to determine the extent to which either mechanism contributes to the "FLASH effect". Following FLASH irradiation, we see no evidence of any crosslink formation; however, FLASH irradiation induces a more anoxic profile of induced damage, supporting the TOD mechanism. Furthermore, treatment of WB-PBLs pre-irradiation with BSO abrogates the reduced strand break damage burden mediated by FLASH exposures. In summary, we do not see any experimental evidence to support the RRR mechanism contributing to the reduced damage burden induced by FLASH. However, the observation of a greater anoxic profile of damage following FLASH irradiation, together with the BSO abrogation of the reduced strand break damage burden mediated by FLASH, lends further support to TOD being a driver of the reduced damage burden plus a change in the damage profile mediated by FLASH.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.