Effects of Extracellular and Intracellular pH on Repair of Potentially Lethal Damage, Chromosome Aberrations and DNA Double-Strand Breaks in Irradiated Plateau-Phase A549 Cells

1994 ◽  
Vol 139 (2) ◽  
pp. 152 ◽  
Author(s):  
Vikram R. Jayanth ◽  
Marian T. Bayne ◽  
Marie E. Varnes
Keyword(s):  
Intracellular Ph ◽  
Chromosome Aberrations ◽  
A549 Cells ◽  
Double Strand Breaks ◽  
Plateau Phase ◽  
Dna Double Strand Breaks ◽  
Strand Breaks ◽  
Lethal Damage

Potentially Lethal Damage, Sublethal Damage and DNA Double Strand Breaks

1985 ◽  
Vol 13 (1-4) ◽  
pp. 171-174 ◽  
Author(s):  
M. Frankenberg-Schwager ◽  
D. Frankenberg ◽  
R. Harbich
Keyword(s):  
Double Strand Breaks ◽  
Dna Double Strand Breaks ◽  
Strand Breaks ◽  
Lethal Damage

scholarly journals Inducible expression and cytogenetic effects of the EcoRI restriction endonuclease in Chinese hamster ovary cells.

1988 ◽  
Vol 8 (10) ◽  
pp. 4204-4211 ◽  
Author(s):  
W F Morgan ◽  
M L Fero ◽  
M C Land ◽  
R A Winegar
Keyword(s):  
Restriction Endonuclease ◽  
Chromosome Aberrations ◽  
Chinese Hamster Ovary Cells ◽  
Chinese Hamster ◽  
Gene Promoter ◽  
Strand Break ◽  
Double Strand Breaks ◽  
Dna Double Strand Breaks ◽  
Bacterial Gene ◽  
Strand Breaks

The cytogenetic endpoints sister chromatid exchange (SCE) and chromosome aberrations are widely used as indicators of DNA damage induced by mutagenic carcinogens. Chromosome aberrations appear to result directly from DNA double-strand breaks, but the lesion(s) giving rise to SCE formation remains unknown. Most compounds that induce SCEs induce a spectrum of lesions in DNA. To investigate the role of double-strand breakage in SCE formation, we constructed a plasmid that gives rise to one specific lesion, a staggered-end ("cohesive") DNA double-strand break. This plasmid, designated pMENs, contains a selectable marker, neo, which is a bacterial gene for neomycin resistance, and the coding sequence for the bacterial restriction endonuclease EcoRI attached to the mouse metallothionein gene promoter. EcoRI recognizes G decreases AATTC sequences in DNA and makes DNA double-strand breaks with four nucleotides overhanging as staggered ends. Cells transfected with pMENS were resistant to the antibiotic G418 and contained an integrated copy of the EcoRI gene, detectable by DNA filter hybridization. The addition of the heavy metal CdSO4 resulted in the intracellular production of EcoRI, as measured by an anti-EcoRI antibody. Cytogenetic analysis after the addition of CdSO4 indicated a dramatic increase in the frequency of chromosome aberrations but very little effect on SCE frequency. Although there was some intercellular heterogeneity, these results confirm that DNA double-strand breaks do result in chromosome aberrations but that these breaks are not sufficient to give rise to SCE formation.

scholarly journals DNA double-strand breaks activate ATM independent of mitochondrial dysfunction in A549 cells

2014 ◽  
Vol 75 ◽  
pp. 30-39 ◽  
Author(s):  
Lidza Kalifa ◽  
Jennifer S. Gewandter ◽  
Rhonda J. Staversky ◽  
Elaine A. Sia ◽  
Paul S. Brookes ◽  
...  
Keyword(s):  
Mitochondrial Dysfunction ◽  
A549 Cells ◽  
Double Strand Breaks ◽  
Dna Double Strand Breaks ◽  
Strand Breaks

Relationships among cytotoxicity, lysosomal breakdown, chromosome aberrations, and DNA double-strand breaks

1987 ◽  
Vol 189 (1) ◽  
pp. 69-79 ◽  
Author(s):  
Matthews O. Bradley ◽  
Victoria I. Taylor ◽  
Michael J. Armstrong ◽  
Sheila M. Galloway
Keyword(s):  
Chromosome Aberrations ◽  
Double Strand Breaks ◽  
Dna Double Strand Breaks ◽  
Strand Breaks

Inducible expression and cytogenetic effects of the EcoRI restriction endonuclease in Chinese hamster ovary cells

1988 ◽  
Vol 8 (10) ◽  
pp. 4204-4211
Author(s):  
W F Morgan ◽  
M L Fero ◽  
M C Land ◽  
R A Winegar
Keyword(s):  
Restriction Endonuclease ◽  
Chromosome Aberrations ◽  
Chinese Hamster Ovary Cells ◽  
Chinese Hamster ◽  
Gene Promoter ◽  
Strand Break ◽  
Double Strand Breaks ◽  
Dna Double Strand Breaks ◽  
Bacterial Gene ◽  
Strand Breaks

The cytogenetic endpoints sister chromatid exchange (SCE) and chromosome aberrations are widely used as indicators of DNA damage induced by mutagenic carcinogens. Chromosome aberrations appear to result directly from DNA double-strand breaks, but the lesion(s) giving rise to SCE formation remains unknown. Most compounds that induce SCEs induce a spectrum of lesions in DNA. To investigate the role of double-strand breakage in SCE formation, we constructed a plasmid that gives rise to one specific lesion, a staggered-end ("cohesive") DNA double-strand break. This plasmid, designated pMENs, contains a selectable marker, neo, which is a bacterial gene for neomycin resistance, and the coding sequence for the bacterial restriction endonuclease EcoRI attached to the mouse metallothionein gene promoter. EcoRI recognizes G decreases AATTC sequences in DNA and makes DNA double-strand breaks with four nucleotides overhanging as staggered ends. Cells transfected with pMENS were resistant to the antibiotic G418 and contained an integrated copy of the EcoRI gene, detectable by DNA filter hybridization. The addition of the heavy metal CdSO4 resulted in the intracellular production of EcoRI, as measured by an anti-EcoRI antibody. Cytogenetic analysis after the addition of CdSO4 indicated a dramatic increase in the frequency of chromosome aberrations but very little effect on SCE frequency. Although there was some intercellular heterogeneity, these results confirm that DNA double-strand breaks do result in chromosome aberrations but that these breaks are not sufficient to give rise to SCE formation.

Potentially Lethal Damage, Sublethal Damage and DNA Double Strand Breaks

1985 ◽  
Vol 13 (1-4) ◽  
pp. 171-174 ◽  
Author(s):  
M. Frankenberg-Schwager ◽  
D. Frankenberg ◽  
R. Harbich
Keyword(s):  
Double Strand Breaks ◽  
Dna Double Strand Breaks ◽  
Strand Breaks ◽  
Lethal Damage

scholarly journals Low Repair Capacity of DNA Double-Strand Breaks Induced by Laser-Driven Ultrashort Electron Beams in Cancer Cells

2020 ◽  
Vol 21 (24) ◽  
pp. 9488
Author(s):  
Nelly Babayan ◽  
Natalia Vorobyeva ◽  
Bagrat Grigoryan ◽  
Anna Grekhova ◽  
Margarita Pustovalova ◽  
...  
Keyword(s):  
Electron Energy ◽  
Ultrashort Pulse ◽  
Electron Beams ◽  
A549 Cells ◽  
Double Strand Breaks ◽  
Pulse Irradiation ◽  
Dna Double Strand Breaks ◽  
Continuous Irradiation ◽  
Strand Breaks ◽  
Γh2ax Foci

Laser-driven accelerators allow to generate ultrashort (from femto- to picoseconds) high peak dose-rate (up to tens of GGy/s) accelerated particle beams. However, the radiobiological effects of ultrashort pulsed irradiation are still poorly studied. The aim of this work was to compare the formation and elimination of γH2AX and 53BP1 foci (well known markers for DNA double-strand breaks (DSBs)) in Hela cells exposed to ultrashort pulsed electron beams generated by Advanced Research Electron Accelerator Laboratory (AREAL) accelerator (electron energy 3.6 MeV, pulse duration 450 fs, pulse repetition rates 2 or 20 Hz) and quasi-continuous radiation generated by Varian accelerator (electron energy 4 MeV) at doses of 250–1000 mGy. Additionally, a study on the dose–response relationships of changes in the number of residual γH2AX foci in HeLa and A549 cells 24 h after irradiation at doses of 500–10,000 mGy were performed. We found no statistically significant differences in γH2AX and 53BP1 foci yields at 1 h after exposure to 2 Hz ultrashort pulse vs. quasi-continuous radiations. In contrast, 20 Hz ultrashort pulse irradiation resulted in 1.27-fold higher foci yields as compared to the quasi-continuous one. After 24 h of pulse irradiation at doses of 500–10,000 mGy the number of residual γH2AX foci in Hela and A549 cells was 1.7–2.9 times higher compared to that of quasi-continuous irradiation. Overall, the obtained results suggest the slower repair rate for DSBs induced by ultrashort pulse irradiation in comparison to DSBs induced by quasi-continuous irradiation.

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