DNA single-strand breaks, double-strand breaks, and crosslinks in rat testicular germ cells: Measurements of their formation and repair by alkaline and neutral filter elution

1985 ◽  
Vol 1 (3) ◽  
pp. 181-195 ◽  
Author(s):  
Matthews O. Bradley ◽  
Gary Dysart
Keyword(s):  
Germ Cells ◽  
Double Strand Breaks ◽  
Single Strand ◽  
Strand Breaks ◽  
Single Strand Breaks

scholarly journals DNA DAMAGE AND REPAIR IN EUKARYOTIC CELLS

Genetics ◽  
1974 ◽  
Vol 78 (1) ◽  
pp. 139-148
Author(s):  
R B Painter
Keyword(s):  
Ionizing Radiation ◽  
Excision Repair ◽  
Double Strand Breaks ◽  
Single Strand ◽  
Premature Aging ◽  
Cross Linking ◽  
Base Damage ◽  
Strand Breaks ◽  
Single Strand Breaks ◽  
Post Replication Repair

ABSTRACT Damage in DNA after irradiation can be classified into five kinds: base damage, single-strand breaks, double-strand breaks, DNA-DNA cross-linking, and DNA-protein cross-linking. Of these, repair of base damage is the best understood. In eukaryotes, at least three repair systems are known that can deal with base damage: photoreactivation, excision repair, and post-replication repair. Photoreactivation is specific for UV-induced damage and occurs widely throughout the biosphere, although it seems to be absent from placental mammals. Excision repair is present in prokaryotes and in animals but does not seem to be present in plants. Post-replication repair is poorly understood. Recent reports indicate that growing points in mammalian DNA simply skip past UV-induced lesions, leaving gaps in newly made DNA that are subsequently filled in by de novo synthesis. Evidence that this concept is oversimplified or incorrect is presented.—Single-strand breaks are induced by ionizing radiation but most cells can rapidly repair most or all of them, even after supralethal doses. The chemistry of the fragments formed when breaks are induced by ionizing radiation is complex and poorly understood. Therefore, the intermediate steps in the repair of single-strand breaks are unknown. Double-strand breaks and the two kinds of cross-linking have been studied very little and almost nothing is known about their mechanisms for repair.—The role of mammalian DNA repair in mutations is not known. Although there is evidence that defective repair can lead to cancer and/or premature aging in humans, the relationship between the molecular defects and the diseased state remains obscure.

Matching of single-strand breaks to form double-strand breaks in DNA

Biopolymers ◽  
1969 ◽  
Vol 7 (5) ◽  
pp. 681-693 ◽  
Author(s):  
David Freifelder ◽  
Bruce Trumbo
Keyword(s):  
Double Strand Breaks ◽  
Single Strand ◽  
Strand Breaks ◽  
Single Strand Breaks

scholarly journals Artificial and Solar UV Radiation Induces Strand Breaks and Cyclobutane Pyrimidine Dimers in Bacillus subtilis Spore DNA

2000 ◽  
Vol 66 (1) ◽  
pp. 199-205 ◽  
Author(s):  
Tony A. Slieman ◽  
Wayne L. Nicholson
Keyword(s):  
Bacillus Subtilis ◽  
Uv Irradiation ◽  
Double Strand Breaks ◽  
Single Strand ◽  
Complex Spectrum ◽  
Cyclobutane Pyrimidine Dimers ◽  
Strand Breaks ◽  
Single Strand Breaks ◽  
Pyrimidine Dimers ◽  
Solar Uv

ABSTRACT The loss of stratospheric ozone and the accompanying increase in solar UV flux have led to concerns regarding decreases in global microbial productivity. Central to understanding this process is determining the types and amounts of DNA damage in microbes caused by solar UV irradiation. While UV irradiation of dormant Bacillus subtilis endospores results mainly in formation of the “spore photoproduct” 5-thyminyl-5,6-dihydrothymine, genetic evidence indicates that an additional DNA photoproduct(s) may be formed in spores exposed to solar UV-B and UV-A radiation (Y. Xue and W. L. Nicholson, Appl. Environ. Microbiol. 62:2221–2227, 1996). We examined the occurrence of double-strand breaks, single-strand breaks, cyclobutane pyrimidine dimers, and apurinic-apyrimidinic sites in spore DNA under several UV irradiation conditions by using enzymatic probes and neutral or alkaline agarose gel electrophoresis. DNA from spores irradiated with artificial 254-nm UV-C radiation accumulated single-strand breaks, double-strand breaks, and cyclobutane pyrimidine dimers, while DNA from spores exposed to artificial UV-B radiation (wavelengths, 290 to 310 nm) accumulated only cyclobutane pyrimidine dimers. DNA from spores exposed to full-spectrum sunlight (UV-B and UV-A radiation) accumulated single-strand breaks, double-strand breaks, and cyclobutane pyrimidine dimers, whereas DNA from spores exposed to sunlight from which the UV-B component had been removed with a filter (“UV-A sunlight”) accumulated only single-strand breaks and double-strand breaks. Apurinic-apyrimidinic sites were not detected in spore DNA under any of the irradiation conditions used. Our data indicate that there is a complex spectrum of UV photoproducts in DNA of bacterial spores exposed to solar UV irradiation in the environment.

UV-induzierte Brüche in 5-Bromuracil-substituierter DNS des Phagen T1 / UV-Induced Strand Breaks in 5-Bromouracil Substituted DNA of Phage T1

1970 ◽  
Vol 25 (9) ◽  
pp. 1037-1042 ◽  
Author(s):  
G. Stephan ◽  
H. G. Miltenburger ◽  
G. Hotz
Keyword(s):  
Biological Activity ◽  
Uv Irradiation ◽  
Uv Light ◽  
Double Strand Breaks ◽  
Single Strand ◽  
Radical Scavenger ◽  
Strand Breaks ◽  
Single Strand Breaks ◽  
Phage Dna ◽  
Site Of Action

Phage Tl and BU-Τ1 (phage DNA substituted with 5-bromouracil) were inactivated by UV-light (2537 A). After irradiation DNA was extracted and its sedimentation behaviour studied by zone centrifugation in neutral and alkaline sucrose gradients, respectively. In the DNA of unsubstituted phage no double-strand breaks and only a small number of single-strand breaks per inactivation dose could be detected after high UV-doses. However, after irradiation of phage BU-T1 double- and single-strand breaks were observed at an increased rate. UV-irradiation in the presence of a radical scavenger (0.01 M cysteamine) prevented the occurrence of double- but not of single strand breaks. The relevance of these breaks attributable to BU-incorporation for the biological activity (plaque forming ability) of the phage and the site of action of cysteamine are discussed.

Change in DNA after Exposure to Hydrogen Atoms.

1969 ◽  
Vol 24 (12) ◽  
pp. 1565-1573 ◽  
Author(s):  
H. Jung, ◽  
U. Hagen, ◽  
M. Ullrich, ◽  
E. E. Petersen
Keyword(s):  
Hydrogen Bonds ◽  
Double Strand Breaks ◽  
Single Strand ◽  
Dna Double Strand Breaks ◽  
Hydrogen Atoms ◽  
Γ Irradiation ◽  
Base Damage ◽  
Strand Breaks ◽  
Single Strand Breaks ◽  
Single Breaks

The action of hydrogen atoms — generated in an electrodeless high frequency gas discharge — on calf thymus DNA in aqueous solution was investigated. The loss of priming activity was compared with the appearance of single strand breaks in native and denatured DNA, double strand breaks, denatured zones, base damage and rupture of hydrogen bonds. The primary lesions after exposure to H atoms and gamma radiation, respectively, are single strand breaks and base damage. Double strand breaks originating from accumulation of single breaks, and rupture of hydrogen bonds caused by single breaks and base damage, were identified as secondary lesions. In relation to strand breaks arising from radical attack on the sugar-phosphate backbone of the DNA molecule, base damage is about 12.5 times more frequent after Η-exposure than after γ-irradiation. It is concluded from this observation, that single strand breaks are the predominant critical lesions responsible for the loss of the functional activity of DNA.

Delayed repletion of O6-methylguanine—DNA methyltransferase resulting in failure to protect the human glioblastoma cell line SF767 from temozolomide-induced cytotoxicity

2003 ◽  
Vol 98 (3) ◽  
pp. 591-598 ◽  
Author(s):  
Yuichi Hirose ◽  
Emiko L. Kreklau ◽  
Leonard C. Erickson ◽  
Mitchel S. Berger ◽  
Russell O. Pieper
Keyword(s):  
Cell Death ◽  
Dna Methyltransferase ◽  
Glioma Cells ◽  
Double Strand Breaks ◽  
Single Strand ◽  
Dna Double Strand Breaks ◽  
Content Type ◽  
Strand Breaks ◽  
Single Strand Breaks ◽  
Fine Print

Object. Temozolomide (TMZ)-induced O6-methylguanine (MG) DNA lesions, if not removed by MG—DNA methyltransferase (MGMT), mispair with thymine, trigger rounds of futile mismatch repair (MMR), and in glioma cells lead to prolonged G2—M arrest and ultimately cell death. Depletion of MGMT by O6-benzylguanine (BG) sensitizes tumor cells to TMZ, and this combination is currently used in clinical trials. The use of the TMZ+BG combination in gliomas, however, is complicated by the prolonged TMZ-induced G2—M arrest, which may delay activation of poorly defined cell death pathways and allow for MGMT repletion and reversal of toxicity. Methods. To address these issues, the actions of TMZ were monitored in DNA MMR-proficient SF767 glioma cells depleted of MGMT by BG, and in cells in which BG was removed at various times after TMZ exposure. In MGMT-depleted cells, TMZ exposure led to DNA single-strand breaks and phosphorylation of cdc2, followed by G2—M arrest, induction of p53/p21, and DNA double-strand breaks. Although DNA single-strand breaks, phosphorylation of cdc2, and G2—M arrest could be reversed by repletion of MGMT up to 5 days after TMZ exposure, TMZ-induced cytotoxicity could only be prevented if MGMT was replenished within 24 hours of the onset of G2—M arrest, and before the creation of DNA double-strand breaks. Conclusions. These results indicate that although SF767 glioma cells undergo a prolonged G2—M arrest in response to TMZ, their ability to escape TMZ-induced cytotoxicity by MGMT repletion is limited to an approximately 24-hour period after the onset of G2—M arrest.

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