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Updated: Jun 24, 2026
06:47
One-step Protocol for Evaluation of the Mode of Radiation-induced Clonogenic Cell Death by Fluorescence Microscopy
Published on: October 23, 2017
[Adaptive response in the different mitotic cycles after irradiation]
Tsitologiia
|March 14, 2009
Summary
Irradiated human lymphocytes exhibit genomic instability and adaptive responses up to the third cell division. DNA double-strand breaks may signal the induction of this adaptive response.
Area of Science:
- Cellular and Molecular Biology
- Radiation Biology
- Genetics
Context:
- Investigating the long-term effects of radiation exposure on human lymphocytes.
- Examining the phenomenon of adaptive response (AR) in non-irradiated cells following parental irradiation.
- Utilizing metaphase analysis and the DNA comet assay to assess chromosomal damage and DNA fragmentation.
Purpose:
- To determine the frequency and type of chromosome aberrations in the progeny of irradiated human blood lymphocytes.
- To quantify DNA fragmentation (double-strand breaks) in these cells using the DNA comet assay.
- To elucidate the temporal dynamics and extent of the adaptive response (AR) in relation to mitotic cycles and DNA damage.
Summary:
- Human lymphocytes exposed to adaptive (0.05 Gy) and challenge (1 Gy) radiation doses showed increased chromosome aberrations and DNA double-strand breaks across mitotic cycles.
- The adaptive response (AR), characterized by reduced aberrations and DNA fragmentation, was observed in the first and second mitotic cycles (48-72 hours post-stimulation) in most individuals.
- Genomic instability was evident in non-irradiated lymphocyte progeny, with the AR being transient, absent by the third/fourth mitosis, and potentially signaled by double-strand DNA breaks.
Impact:
- Provides insights into the complex interplay between radiation-induced DNA damage and cellular repair mechanisms.
- Highlights the transient nature of the adaptive response in human lymphocytes, offering a more nuanced understanding of radio-protection.
- Suggests a potential signaling role for double-strand DNA breaks in initiating adaptive responses, relevant for radiation protection strategies.
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