Physical interaction ionising radiations with the intracellular macromolecular target DNA and its biological consequences

C. R. Geard, Bradford Loucas

Research output: Contribution to journalArticle

Abstract

Chromosomal DNA breaks were evaluated in normal human fibroblasts after irradiation of non-cycling G1 phase cells with 90 keV.μm -1 α a particles and 250 kV(p) X rays. Yields were measured using the premature chromosome condensation technique in interphase cells, straight after and 24 h after irradiation, and by mitotic scoring of terminal deletions following cellular release at 24 h and progression through the cell cycle. Yields were related to the frequencies of energy deposition events per cell nucleus estimated microdosimetrically for X rays and by relating fluence to nuclear cross-sectional areas for the a particles. Linear relationships were found for both radiations and at all three times post-irradiation. Initial break yields of 1.3 x 10 0 and 1.6 x 10 -2 per energy deposition event for a particles and X rays respectively, changed to residual yields (24 h) of 4.0 x 10 -1 and 1.3 x 10 -3, and for terminal deletions at mitosis to 6.0 x 10 -3 and 4.0 x 10 -5 per energy deposition event. That is, one 90 keV.μm -1 a particle is about 100 times more biologically effective than an electron track from 250 kV(p) X rays and greater than 99% of initially induced chromosomal DNA breaks are repaired/misrepaired before the next mitosis. Misrepair will involve illegitimate interactions and combinations of pairs of lesions, entities which pre-dominate at mitosis, while a failure to repair/misrepair resulting in relic DNA double strand breaks is likely to be of minimal consequence. Lesion interaction, proximity dependent, and largely irrespective of LET dependent lesion severity will then be the principal basis for the unwanted biological sequelae from ionising radiations.

Original languageEnglish (US)
Pages (from-to)101-106
Number of pages6
JournalRadiation Protection Dosimetry
Volume61
Issue number1-3
StatePublished - 1995
Externally publishedYes

Fingerprint

Ionizing radiation
Ionizing Radiation
mitosis
ionizing radiation
DNA
deoxyribonucleic acid
Mitosis
X-Rays
lesions
Chromosome Breakage
X rays
deletion
DNA Breaks
Irradiation
irradiation
x rays
Cells
interactions
Linear Energy Transfer
Double-Stranded DNA Breaks

ASJC Scopus subject areas

  • Radiology Nuclear Medicine and imaging
  • Radiological and Ultrasound Technology
  • Nuclear Energy and Engineering
  • Radiation

Cite this

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abstract = "Chromosomal DNA breaks were evaluated in normal human fibroblasts after irradiation of non-cycling G1 phase cells with 90 keV.μm -1 α a particles and 250 kV(p) X rays. Yields were measured using the premature chromosome condensation technique in interphase cells, straight after and 24 h after irradiation, and by mitotic scoring of terminal deletions following cellular release at 24 h and progression through the cell cycle. Yields were related to the frequencies of energy deposition events per cell nucleus estimated microdosimetrically for X rays and by relating fluence to nuclear cross-sectional areas for the a particles. Linear relationships were found for both radiations and at all three times post-irradiation. Initial break yields of 1.3 x 10 0 and 1.6 x 10 -2 per energy deposition event for a particles and X rays respectively, changed to residual yields (24 h) of 4.0 x 10 -1 and 1.3 x 10 -3, and for terminal deletions at mitosis to 6.0 x 10 -3 and 4.0 x 10 -5 per energy deposition event. That is, one 90 keV.μm -1 a particle is about 100 times more biologically effective than an electron track from 250 kV(p) X rays and greater than 99{\%} of initially induced chromosomal DNA breaks are repaired/misrepaired before the next mitosis. Misrepair will involve illegitimate interactions and combinations of pairs of lesions, entities which pre-dominate at mitosis, while a failure to repair/misrepair resulting in relic DNA double strand breaks is likely to be of minimal consequence. Lesion interaction, proximity dependent, and largely irrespective of LET dependent lesion severity will then be the principal basis for the unwanted biological sequelae from ionising radiations.",
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T1 - Physical interaction ionising radiations with the intracellular macromolecular target DNA and its biological consequences

AU - Geard, C. R.

AU - Loucas, Bradford

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N2 - Chromosomal DNA breaks were evaluated in normal human fibroblasts after irradiation of non-cycling G1 phase cells with 90 keV.μm -1 α a particles and 250 kV(p) X rays. Yields were measured using the premature chromosome condensation technique in interphase cells, straight after and 24 h after irradiation, and by mitotic scoring of terminal deletions following cellular release at 24 h and progression through the cell cycle. Yields were related to the frequencies of energy deposition events per cell nucleus estimated microdosimetrically for X rays and by relating fluence to nuclear cross-sectional areas for the a particles. Linear relationships were found for both radiations and at all three times post-irradiation. Initial break yields of 1.3 x 10 0 and 1.6 x 10 -2 per energy deposition event for a particles and X rays respectively, changed to residual yields (24 h) of 4.0 x 10 -1 and 1.3 x 10 -3, and for terminal deletions at mitosis to 6.0 x 10 -3 and 4.0 x 10 -5 per energy deposition event. That is, one 90 keV.μm -1 a particle is about 100 times more biologically effective than an electron track from 250 kV(p) X rays and greater than 99% of initially induced chromosomal DNA breaks are repaired/misrepaired before the next mitosis. Misrepair will involve illegitimate interactions and combinations of pairs of lesions, entities which pre-dominate at mitosis, while a failure to repair/misrepair resulting in relic DNA double strand breaks is likely to be of minimal consequence. Lesion interaction, proximity dependent, and largely irrespective of LET dependent lesion severity will then be the principal basis for the unwanted biological sequelae from ionising radiations.

AB - Chromosomal DNA breaks were evaluated in normal human fibroblasts after irradiation of non-cycling G1 phase cells with 90 keV.μm -1 α a particles and 250 kV(p) X rays. Yields were measured using the premature chromosome condensation technique in interphase cells, straight after and 24 h after irradiation, and by mitotic scoring of terminal deletions following cellular release at 24 h and progression through the cell cycle. Yields were related to the frequencies of energy deposition events per cell nucleus estimated microdosimetrically for X rays and by relating fluence to nuclear cross-sectional areas for the a particles. Linear relationships were found for both radiations and at all three times post-irradiation. Initial break yields of 1.3 x 10 0 and 1.6 x 10 -2 per energy deposition event for a particles and X rays respectively, changed to residual yields (24 h) of 4.0 x 10 -1 and 1.3 x 10 -3, and for terminal deletions at mitosis to 6.0 x 10 -3 and 4.0 x 10 -5 per energy deposition event. That is, one 90 keV.μm -1 a particle is about 100 times more biologically effective than an electron track from 250 kV(p) X rays and greater than 99% of initially induced chromosomal DNA breaks are repaired/misrepaired before the next mitosis. Misrepair will involve illegitimate interactions and combinations of pairs of lesions, entities which pre-dominate at mitosis, while a failure to repair/misrepair resulting in relic DNA double strand breaks is likely to be of minimal consequence. Lesion interaction, proximity dependent, and largely irrespective of LET dependent lesion severity will then be the principal basis for the unwanted biological sequelae from ionising radiations.

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