Ionizing Radiation Repair
Ionizing Radiation Repair - Related Videos
09:28
Evaluation of the Spatial Distribution of γH2AX following Ionizing Radiation
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Cited by 7 •
2010
Microscopic analysis of γH2AX foci, which form following the phosphorylation of H2AX at Ser-139 in response to DNA double-strand breaks, has become an invaluable tool in radiation biology. Here we used an antibody to mono-methylated histone H3 at lysine 4 as an epigenetic marker of actively transcribing euchromatin, to evaluate the spatial distribution of radiation-induced γH2AX formation within the nucleus.
06:21
Diffuse Optical Spectroscopy for the Quantitative Assessment of Acute Ionizing Radiation Induced Skin Toxicity Using a Mouse Model
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Cited by 13 •
2016
We present a diffuse optical spectroscopic (DOS) approach that provides quantitative optical biomarkers of skin response to radiation. We describe DOS instrumentation design, optical parameters extraction algorithms and the animal handling procedures required to yield representative data from a pre-clinical mouse model of radiation induced erythema.
02:59
Biological Effects of Radiation
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2020
All radioactive nuclides emit high-energy particles or electromagnetic waves. When this radiation encounters living cells, it can cause heating, break chemical bonds, or ionize molecules. The most serious biological damage results when these radioactive emissions fragment or ionize molecules. For example, α and β particles emitted from nuclear decay reactions possess much higher energies than ordinary chemical bond energies. When these particles strike and penetrate matter, they produce ions...
11:24
Measuring DNA Damage and Repair in Mouse Splenocytes After Chronic In Vivo Exposure to Very Low Doses of Beta- and Gamma-Radiation
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Cited by 3 •
2015
A protocol to evaluate changes in DNA damage levels and DNA repair capacity that may be induced by chronic in vivo low dose irradiation in mouse spleen lymphocytes, by measuring phosphorylated histone H2AX, a marker of DNA double-strand breaks, using flow cytometry is presented.
01:02
Long-patch Base Excision Repair
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2020
Since the discovery of the two BER pathways, there has been a debate about how a cell chooses one pathway over the other and the factors determining this selection. Numerous in vitro experiments have pointed out multiple determinants for the sub-pathway selection. These are: Lesion type: Depending on the type of base damage, a specific DNA glycosylase - mono or bifunctional, is recruited to the damaged site. While the sequential action of a monofunctional glycosylase favors long patch repair...
FAQs
Damage-sensing proteins provide the initial recognition step after radiation-induced lesions arise. Their activation is linked to cell-cycle checkpoints, which connect DNA damage detection with control of cellular progression. This coordination gives repair pathways an opportunity to act before genome instability becomes established, making the sensing-checkpoint relationship central to understanding cellular survival after exposure.
Non-homologous end joining and homologous recombination are identified as major repair pathways in the response to radiation-associated DNA breaks. Considering both is important because ionizing radiation can produce single- and double-strand breaks, and repair research must relate lesion type to pathway activation. Their study helps explain how cells preserve genome stability after exposure.
Radiation damage has outcomes beyond successful correction. If lesions are not properly resolved, the resulting loss of genetic integrity can contribute to mutation, while extensive damage can be associated with cell death. Examining this range of outcomes helps explain why the same physical stress can produce survival in some cells and elimination in others.
Comparing tumors with normal tissues is a central biological context for radiation response. Differences in how these cell populations respond to damage and repair can influence radiotherapy outcomes, because treatment seeks to affect tumor cells while limiting injury to normal tissue. Ionizing Radiation Repair research therefore links molecular damage responses with tissue-level treatment effects.
Radiation protection uses repair biology to understand how exposure affects genome stability and cell survival. Studying damage detection, checkpoint activation, and repair pathways can clarify the cellular consequences of ionizing radiation, supporting efforts to evaluate and reduce biological harm. The relevance extends beyond treatment because the same response mechanisms matter when radiation is considered as a hazard.
Research on inherited repair deficiencies examines what happens when systems that respond to radiation damage do not function normally. Such studies can connect impaired genome maintenance with altered mutation or cell-survival outcomes. They also provide a biological context for understanding why repair capacity matters in disease research and why inherited defects are relevant to radiation responses.