Radiosensitivity

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Radiosensitivity is the relative susceptibility of cells, tissues, organs or organisms to the harmful effect of ionizing radiation.

Cells types affected

Cells are least sensitive when in the

X-rays are more effective on cells which have a greater reproductive activity.[1][2]

From their observations, they concluded that quickly dividing

free radicals
produced by ionizing oxygen.

It has meanwhile been shown that the most sensitive cells are those that are

muscle fibers
.

Very sensitive cells are also oocytes and lymphocytes, although they are resting cells and do not meet the criteria described above. The reasons for their sensitivity are not clear.

There also appears to be a genetic basis for the varied vulnerability of cells to ionizing radiation.[4] This has been demonstrated across several cancer types and in normal tissues.[5][6]

Cell damage classification

The damage to the cell can be lethal (the cell dies) or sublethal (the cell can repair itself). Cell damage can ultimately lead to health effects which can be classified as either Tissue Reactions or Stochastic Effects according to the International Commission on Radiological Protection.

Tissue reactions

Tissue reactions have a threshold of irradiation under which they do not appear and above which they typically appear. Fractionation of dose, dose rate, the application of antioxidants and other factors may affect the precise threshold at which a tissue reaction occurs. Tissue reactions include skin reactions (epilation, erythema, moist desquamation), cataracts, circulatory disease, and other conditions. Seven proteins were discovered in a systematic review, which correlated with radiosensitivity in normal tissues: γH2AX, TP53BP1, VEGFA, CASP3, CDKN2A, IL6, and IL1B.[7][8]

Stochastic effects

Stochastic effects do not have a threshold of irradiation, are coincidental, and cannot be avoided. They can be divided into somatic and genetic effects. Among the somatic effects, secondary cancer is the most important. It develops because radiation causes DNA mutations directly and indirectly. Direct effects are those caused by ionizing particles and rays themselves, while the indirect effects are those that are caused by free radicals, generated especially in water radiolysis and oxygen radiolysis. The genetic effects confer the predisposition of radiosensitivity to the offspring.[9] The process is not well understood yet.

Target structures

For decades, the main cellular target for radiation induced damage was thought to be the DNA molecule.[10] This view has been challenged by data indicating that in order to increase survival, the cells must protect their proteins, which in turn repair the damage in the DNA.[11] An important part of protection of proteins (but not DNA) against the detrimental effects of reactive oxygen species (ROS), which are the main mechanism of radiation toxicity, is played by non-enzymatic complexes of manganese ions and small organic metabolites.[11] These complexes were shown to protect the proteins from oxidation in vitro[12] and also increased radiation survival in mice.[13] An application of the synthetically reconstituted protective mixture with manganese was shown to preserve the immunogenicity of viral and bacterial epitopes at radiation doses far above those necessary to kill the microorganisms, thus opening a possibility for a quick whole-organism vaccine production.[14] The intracellular manganese content and the nature of complexes it forms (both measurable by electron paramagnetic resonance) were shown to correlate with radiosensitivity in bacteria, archaea, fungi and human cells.[15] An association was also found between total cellular manganese contents and their variation, and clinically inferred radioresponsiveness in different tumor cells, a finding that may be useful for more precise radiodosages and improved treatment of cancer patients.[16]

See also

References

  1. ^ Bergonié J, Tribondeau L (1906). "De Quelques Résultats de la Radiotherapie et Essai de Fixation d'une Technique Rationnelle". Comptes Rendus des Séances de l'Académie des Sciences. 143: 983–985.
  2. JSTOR 3570812
    .
  3. PMID 13000583
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  4. S2CID 91187501
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  5. PMID 27109210
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  6. PMID 22169268
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  7. PMID 33669522
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  8. PMID 33375047
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  9. doi:10.1504/IJLR.2016.10002388
    .
  10. PMID 5924966
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  11. ^
    S2CID 17787568
    .
  12. PMID 20838443
    .
  13. PMID 27500529
    .
  14. PMID 22817993
    .
  15. PMID 29042516
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  16. PMID 30027971
    .
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