scholarly journals Comparative Studies on Protective Effect of Various Sulfhydryl Compounds Against Cell Death and DNA Strand Breaks Induced by X-Rays in Cultured Mouse L Cells

1978 ◽  
Vol 19 (4) ◽  
pp. 319-335 ◽  
Author(s):  
T. MORI ◽  
M. HORIKAWA ◽  
O. NIKAIDO ◽  
T. SUGAHARA
Keyword(s):  
Cell Death ◽  
Protective Effect ◽  
Comparative Studies ◽  
Dna Strand Breaks ◽  
X Rays ◽  
Strand Breaks ◽  
L Cells ◽  
Dna Strand ◽  
Sulfhydryl Compounds

scholarly journals Resolution of DNA damage at the single-cell level shows largely different actions of X-rays and bleomycin.

1995 ◽  
Vol 43 (2) ◽  
pp. 229-235 ◽  
Author(s):  
M I Affentranger ◽  
W Burkart
Keyword(s):  
Single Cell ◽  
Cell Population ◽  
Large Cell ◽  
Dna Strand Breaks ◽  
Single Cell Level ◽  
X Rays ◽  
Cell Level ◽  
Strand Breaks ◽  
Two Agents ◽  
Dna Strand

Both X-rays and the radiomimetic agent bleomycin (BLM) induce DNA strand breaks, predominantly via reactive radicals. To compare the induction of breaks with the two agents in Chinese hamster (CHO-K1) cells, two different alkaline unwinding methods, a 3H tracer-based analysis of large cell populations and an optical adaption allowing measurement of single cells, were applied. Radiation and BLM show qualitatively similar dose responses when the average number of DNA strand breaks is measured in a large cell population. However, the breakage pattern at the single-cell level indicates large discrepancies between the actions of the two agents. Irradiated cells show a uniform distribution of DNA strand breaks over the cell population. Effects of treatment with 30 micrograms x ml-1 BLM for 2 hr vary from practically zero in some cells to high levels of DNA strand breakage in others. Unlike the repair of radiation-induced DNA breaks, the repair efficiency of BLM-induced DNA strand breaks, as measured at the single-cell level, varies strongly among cells of the same population. Such heterogeneity at the cellular level potentially reduces BLM's usefulness for tumor therapy because the appearance of BLM-resistant subpopulations may critically impair treatment outcome.

Protective effect of magnesium on DNA strand breaks induced by nickel or cadmium

1994 ◽  
Vol 10 (2) ◽  
pp. 127-135 ◽  
Author(s):  
N. A. Littlefield ◽  
B. S. Hass ◽  
S. J. James ◽  
L. A. Poirier
Keyword(s):  
Protective Effect ◽  
Dna Strand Breaks ◽  
Strand Breaks ◽  
Dna Strand

Poly(ADP-ribose) polymerase inhibitors as potential chemotherapeutic agents

2004 ◽  
Vol 32 (6) ◽  
pp. 959-961 ◽  
Author(s):  
H.E. Bryant ◽  
T. Helleday
Keyword(s):  
Cell Death ◽  
Dna Repair ◽  
Parp Inhibitor ◽  
Polymerase Activity ◽  
Dna Strand Breaks ◽  
Chemotherapeutic Agents ◽  
Strand Breaks ◽  
Polymerase Inhibitors ◽  
Dna Strand ◽  
Made In

PARP [poly(ADP-ribose) polymerase] activity is up-regulated by binding to DNA strand breaks and its association with DNA repair is well documented. Many anticancer therapies work by inducing breaks in DNA, if unrepaired these can lead to cell death. As PARP promotes DNA repair there is a strong rational to suggest that its inhibition may increase the efficiency of certain cytotoxic treatments. This review discusses the advances made in PARP inhibitor design and the mechanism by which they enhance anti-tumour therapies.

A Molecular Dynamics of Radiation-Induced DNA Damage Response: Exploring the Pathways of Signaling, Repair, and Cell Death

2021 ◽  
Vol 8 (2) ◽  
Author(s):  
Singh V ◽  
◽  
Kumar R ◽  
Gautam HK ◽  
◽  
...  
Keyword(s):  
Dna Damage ◽  
Cell Death ◽  
Signaling Pathways ◽  
Healthcare Providers ◽  
Dna Strand Breaks ◽  
Strand Breaks ◽  
Checkpoint Kinases ◽  
Research Concept ◽  
Dna Strand ◽  
New Research

Purpose: In this review, we summarized the latest information related to accidentally and/or un-accidental exposure of ionizing radiation triggered by oxidative stress and/or cytotoxicity and adverse effects on human health such as hematopoietic, gastrointestinal and cerebrovascular injury collectively referred to as acute radiation syndromes. Directly or indirectly IR induced oxidation of biomolecules, especially DNA, resulting in altered genomic stability and DNA strand breaks. DNA strand breaks are recognized by DNA damage sensory protein that activates downstream checkpoint kinases as well as initiate compensatory multiple intracellular and intranuclear signaling pathways, resulting in cell cycle arrest and DNA repair. Simultaneously activates tumor suppressor genes leading to death signaling pathway or triggering of numerous autocrine/paracrine loops leading to structural dis-organization and programmed cell death. These signaling pathways work together to decrease the magnitude of radiotherapy and promote the development of radiation resistance in cancer cells. The fate of the cells and DNA damage repair depending on the severity of radiation exposure and types of DNA damage. Conclusions: Based on the recent invested reports related to IR and DNA damage signaling, this review would be helpful for researchers and healthcare providers to develop a new research concept and translate this information into a cancer therapeutic approach. Moreover, target specific screening and development of radiation countermeasures agent for radiological emergencies.

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