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Review
. 2021 Jul 2;22(13):7158.
doi: 10.3390/ijms22137158.

Human Radiosensitivity and Radiosusceptibility: What Are the Differences?

Laura El-Nachef  1 , Joelle Al-Choboq  1 , Juliette Restier-Verlet  1 , Adeline Granzotto  1 , Elise Berthel  1   2 , Laurène Sonzogni  1 , Mélanie L Ferlazzo  1 , Audrey Bouchet  1 , Pierre Leblond  3 , Patrick Combemale  3 , Stéphane Pinson  4 , Michel Bourguignon  1   5 , Nicolas Foray  1
Affiliations
Review

Human Radiosensitivity and Radiosusceptibility: What Are the Differences?

Laura El-Nachef et al. Int J Mol Sci. .

Abstract

The individual response to ionizing radiation (IR) raises a number of medical, scientific, and societal issues. While the term "radiosensitivity" was used by the pioneers at the beginning of the 20st century to describe only the radiation-induced adverse tissue reactions related to cell death, a confusion emerged in the literature from the 1930s, as "radiosensitivity" was indifferently used to describe the toxic, cancerous, or aging effect of IR. In parallel, the predisposition to radiation-induced adverse tissue reactions (radiosensitivity), notably observed after radiotherapy appears to be caused by different mechanisms than those linked to predisposition to radiation-induced cancer (radiosusceptibility). This review aims to document these differences in order to better estimate the different radiation-induced risks. It reveals that there are very few syndromes associated with the loss of biological functions involved directly in DNA damage recognition and repair as their role is absolutely necessary for cell viability. By contrast, some cytoplasmic proteins whose functions are independent of genome surveillance may also act as phosphorylation substrates of the ATM protein to regulate the molecular response to IR. The role of the ATM protein may help classify the genetic syndromes associated with radiosensitivity and/or radiosusceptibility.

Keywords: ATM; ionizing radiation; radiodegeneration; radiosensitivity; radiosusceptibility.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Summary of the major radiosensitive syndromes described in Table 1 and represented by their proteins and their biological role in the cell. There is still no data available to classify radiosensitive syndromes caused by BTK, DNMT3B, and SCID mutations as associated with aging or cancer proneness similar to ATM, LIG4, and NBS1 mutations.
Figure 2
Figure 2
Relationship between radiosensitivity (represented by SF2) and prevalence for the syndromes described in Table 1. Syndromes with only few cases were omitted. Dotted lines represent a data fit to a sigmoidal formula.
Figure 3
Figure 3
Relationships between radiosensitivity, radiosusceptibility, and radiodegeneration throughout the RIANS model and the MRE11 foci kinetics.
See this image and copyright information in PMC

References

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