Uv Radiation Damage
Uv Radiation Damage - Related Videos
04:09
Assessing DNA Damage Foci: To Identify Radiation-Induced DNA Damage Foci in Cancer Cell Line Using Immunofluorescence Staining
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2023
This video describes a protocol to detect radiation-induced DNA repair foci in the colon cancer cell lines using immunofluorescence staining. DNA repair proteins get activated at the DNA damage site; therefore, we can detect them using specific antibodies and visualize them under a fluorescence microscope.
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.
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...
12:59
Assessment of Oxidative Damage in the Primary Mouse Ocular Surface Cells/Stem Cells in Response to Ultraviolet-C (UV-C) Damage
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Cited by 12 •
2020
This protocol demonstrates the simultaneous detection of reactive oxygen species (ROS), live cells, and dead cells in live primary cultures from mouse ocular surface cells. 2',7'-Dichlorofluoresceindiacetate, propidium iodide, and Hoechst staining are used to assess the ROS, dead cells, and live cells, respectively, followed by imaging and analysis.
09:31
Determining the Toxicity of UV Radiation and Chemicals on Primary and Immortalized Human Corneal Epithelial Cells
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Cited by 1 •
2021
This article describes the procedures used to evaluate the toxicity of UV radiation and chemical toxins on a primary and immortalized cell line.
FAQs
UVB and UVA initiate injury through different molecular routes. UVB directly produces covalent links between neighboring pyrimidines, generating cyclobutane pyrimidine dimers and other photoproducts. UVA instead can promote reactive oxygen species, which oxidize cellular components. This distinction helps researchers connect wavelength-specific exposure to different biological stress patterns.
Nucleotide excision repair provides a cellular response to DNA lesions created by UV exposure, including damage associated with UVB photoproducts. Its importance lies in protecting genome stability: successful repair can limit the persistence of lesions, whereas inadequate resolution leaves damage associated with mutation formation. This pathway is therefore central to studying cellular recovery after exposure.
Cell fate depends partly on how severe the injury becomes. After UV exposure, cells may temporarily halt progression through the cell cycle, enter senescence, or undergo apoptosis. These outcomes represent distinct cellular responses, and comparing them helps explain how biological systems respond when DNA repair does not fully resolve the damage.
A focused investigation can compare the initial molecular injury with later cellular responses. Researchers may examine DNA photoproducts, oxidation of cellular components, repair pathways, and changes in cell fate such as arrest, senescence, or apoptosis. Linking these levels helps connect a UV exposure response to genome stability and tissue-related outcomes.
Following the progression from UV-induced lesions to cellular repair or altered cell fate helps clarify how mutations may arise. The same framework connects molecular damage with broader biological consequences, including compromised genome stability, skin aging, and skin cancer. Thus, UV studies can relate an environmental stressor to both immediate cellular responses and longer-term outcomes.
Research identifies which molecular and cellular events should be limited or monitored during ultraviolet exposure. Findings on DNA lesions, reactive oxygen species, repair responses, and severe-damage outcomes can guide photoprotection research without treating protection as a single process. The work also places UV stress within broader studies of environmental responses and mechanisms that preserve genome stability.