Literature DB >> 3306760

Potentially lethal damage repair is due to the difference of DNA double-strand break repair under immediate and delayed plating conditions.

M Frankenberg-Schwager, D Frankenberg, R Harbich.   

Abstract

Cells plated immediately after irradiation on nutrient agar (immediate plating) exhibit a lower survival than cells which are kept under nongrowth conditions before plating (delayed plating). The difference between the survival curves obtained after immediate plating and delayed plating is considered to exhibit the cell's capacity to repair potentially lethal damage. In yeast evidence has been presented previously for the DNA double-strand break (DSB) as the molecular lesion involved in the repair of potentially lethal damage observed at the cellular level. Radiation-induced DSB are repaired in cells plated on nutrient agar, i.e., under growth conditions, as well as in cells kept under nongrowth conditions. In this paper DSB repair under growth and nongrowth conditions is studied with the help of the yeast mutant rad54-3 which is temperature conditional for DSB repair. It is shown that the extent of repair of potentially lethal damage can be varied by shifting the relative fractions of repair of DSB under growth conditions versus nongrowth conditions. Repair of DSB in cells plated on nutrient agar is promoted when glucose is substituted by Na-succinate as an energy source. As a result the immediate plating survival curve approaches the delayed plating survival curve, thus reducing the operationally defined repair of potentially lethal damage. We show that this reduced potentially lethal damage repair is caused, however, by a higher amount of DSB repair in cells immediately plated on succinate agar as compared to glucose agar.

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Year:  1987        PMID: 3306760

Source DB:  PubMed          Journal:  Radiat Res        ISSN: 0033-7587            Impact factor:   2.841


  6 in total

1.  In vitro holding and PLD repair. I. On the contribution of mitotic non-quiescence in plateau-phase Chinese hamster V79 cells.

Authors:  A F Stevenson; C S Lange
Journal:  Radiat Environ Biophys       Date:  1989       Impact factor: 1.925

Review 2.  Induction, repair and biological relevance of radiation-induced DNA lesions in eukaryotic cells.

Authors:  M Frankenberg-Schwager
Journal:  Radiat Environ Biophys       Date:  1990       Impact factor: 1.925

3.  Cyclopamine-loaded core-cross-linked polymeric micelles enhance radiation response in pancreatic cancer and pancreatic stellate cells.

Authors:  Jun Zhao; Chunhui Wu; James Abbruzzese; Rosa F Hwang; Chun Li
Journal:  Mol Pharm       Date:  2015-05-12       Impact factor: 4.939

4.  Differential response of human and rodent cell lines to chemical inhibition of the repair of potentially lethal damage.

Authors:  J B Little; A M Ueno; W K Dahlberg
Journal:  Radiat Environ Biophys       Date:  1989       Impact factor: 1.925

5.  The mitochondria-targeted nitroxide JP4-039 augments potentially lethal irradiation damage repair.

Authors:  Malolan S Rajagopalan; Kanika Gupta; Michael W Epperly; Darcy Franicola; Xichen Zhang; Hong Wang; Hong Zhao; Vladimir A Tyurin; Joshua G Pierce; Valerian E Kagan; Peter Wipf; Anthony J Kanai; Joel S Greenberger
Journal:  In Vivo       Date:  2009 Sep-Oct       Impact factor: 2.155

6.  Evidence against the "oxygen-in-the-track" hypothesis as an explanation for the radiobiological low oxygen enhancement ratio at high linear energy transfer radiation.

Authors:  M Frankenberg-Schwager; D Frankenberg; R Harbich; S Beckonert
Journal:  Radiat Environ Biophys       Date:  1994       Impact factor: 1.925

  6 in total

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