scholarly journals Decreased integrity of exercise-induced plasma cell free nuclear DNA – negative association with the increased oxidants production by circulating phagocytes

2018 ◽  
Author(s):  
Robert Stawski ◽  
Konrad Walczak ◽  
Ewelina Perdas ◽  
Anna Wlodarczyk ◽  
Agata Sarniak ◽  
...  
Keyword(s):  
Nuclear Dna ◽  
Dna Strand Breaks ◽  
Exhaustive Exercise ◽  
Strenuous Exercise ◽  
Dna Integrity ◽  
Exercise Tests ◽  
Mt Dna ◽  
Post Exercise ◽  
Strand Breaks ◽  
Dna Strand

AbstractStrenuous exercise increases circulating cell free DNA (cf DNA) and stimulates blood phagocytes to generate reactive oxygen species (ROS) which may induce DNA strand breaks. We tested whether: (A) elevated cf DNA in response to three repeated bouts of exhaustive exercise has decreased integrity; (B) each bout of exercise increases luminol enhanced whole blood chemiluminescence (LBCL) as a measure of ROS production by polymorphonuclear leukocytes. Eleven men performed three treadmill exercise tests to exhaustion separated by 72 hours of resting. Pre- and post-exercise concentrations and integrity of cf nuclear and mitochondrial DNA (cf n-DNA, cf mt-DNA) and resting and fMLP-stimulated LBCL were determined. Each bout increased concentrations of cf n-DNA by more than 10-times which was accompanied by about 2-times elevated post-exercise rLBCL and fMLP-LBCL. Post-exercise cf n-DNA integrity (integrity index, I206/78) decreased after the first (0.59±0.19 vs. 0.48±0.18) and second (0.53±0.14 vs. 0.44±0.17) bout of exercise. There were negative correlations between I206/78and rLBCL (ƍ=−0.37) and I206/78and fMLP-LBCL (ƍ=− 0.40) – analysis of pooled pre- and post-exercise data (n=66). cf-mt DNA integrity (I218/97) did not alter in response to exercise. This suggests an involvement of phagocyte ROS in cf n-DNA strand breaks in response to exhaustive exercise.

scholarly journals Decreased integrity of exercise-induced plasma cell free nuclear DNA – negative association with the increased oxidants production by circulating phagocytes

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Robert Stawski ◽  
Konrad Walczak ◽  
Ewelina Perdas ◽  
Anna Wlodarczyk ◽  
Agata Sarniak ◽  
...  
Keyword(s):  
Nuclear Dna ◽  
Dna Strand Breaks ◽  
Exhaustive Exercise ◽  
Strenuous Exercise ◽  
Dna Integrity ◽  
Exercise Tests ◽  
Mt Dna ◽  
Post Exercise ◽  
Strand Breaks ◽  
Dna Strand

Abstract Strenuous exercise increases circulating cell free DNA (cfDNA) and stimulates blood phagocytes to generate reactive oxygen species (ROS) which may induce DNA strand breaks. We tested whether: (A) elevated cfDNA in response to three repeated bouts of exhaustive exercise has decreased integrity; (B) each bout of exercise increases luminol enhanced whole blood chemiluminescence (LBCL) as a measure of ROS production by polymorphonuclear leukocytes. Eleven men performed three treadmill exercise tests to exhaustion separated by 72 hours of resting. Pre- and post-exercise concentrations and integrity of cf nuclear and mitochondrial DNA (cf n-DNA, cf mt-DNA) and resting (r) and fMLP (n-formyl-methionyl-leucyl-phenylalanine)-stimulated LBCL were determined. Each bout increased concentrations of cf n-DNA by more than 10-times which was accompanied by about 2-times elevated post-exercise rLBCL and fMLP-LBCL. Post-exercise cf n-DNA integrity (integrity index, I229/97) decreased after the first (0.59 ± 0.19 vs. 0.48 ± 0.18) and second (0.53 ± 0.14 vs. 0.44 ± 0.17) bout of exercise. There were negative correlations between I229/97 and rLBCL (ƍ = –0.37), and I229/97 and fMLP-LBCL (ƍ = –0.40) – analysis of pooled pre- and post-exercise data (n = 66). cf mt- DNA integrity (I218/78) did not alter in response to exercise. This suggests an involvement of phagocyte ROS in cf n-DNA strand breaks in response to exhaustive exercise.

The significance of sperm nuclear DNA strand breaks on reproductive outcome

2005 ◽  
Vol 17 (3) ◽  
pp. 255-260 ◽  
Author(s):  
Marcello Spano ◽  
Emre Seli ◽  
Davide Bizzaro ◽  
Gian Carlo Manicardi ◽  
Denny Sakkas
Keyword(s):  
Nuclear Dna ◽  
Dna Strand Breaks ◽  
Reproductive Outcome ◽  
Strand Breaks ◽  
Dna Strand

scholarly journals Nuclear DNA strand breaks during ethanol-induced oxidative stress in rat brain

FEBS Letters ◽  
1996 ◽  
Vol 390 (2) ◽  
pp. 153-156 ◽  
Author(s):  
M. Renis ◽  
V. Calabrese ◽  
A. Russo ◽  
A. Calderone ◽  
M.L. Barcellona ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Rat Brain ◽  
Nuclear Dna ◽  
Dna Strand Breaks ◽  
Strand Breaks ◽  
Dna Strand

scholarly journals Repair of DNA Strand Breaks by the Overlapping Functions of Lesion-Specific and Non-Lesion-Specific DNA 3′ Phosphatases

2001 ◽  
Vol 21 (21) ◽  
pp. 7191-7198 ◽  
Author(s):  
John R. Vance ◽  
Thomas E. Wilson
Keyword(s):  
Dna Damage ◽  
Oxidative Dna Damage ◽  
Synthetic Lethality ◽  
Dna Strand Breaks ◽  
Triple Mutant ◽  
Phosphatase Domain ◽  
Strand Breaks ◽  
Alternative Pathways ◽  
Processing Enzymes ◽  
Dna Strand

ABSTRACT In Saccharomyces cerevisiae, the apurinic/apyrimidinic (AP) endonucleases Apn1 and Apn2 act as alternative pathways for the removal of various 3′-terminal blocking lesions from DNA strand breaks and in the repair of abasic sites, which both result from oxidative DNA damage. Here we demonstrate that Tpp1, a homologue of the 3′ phosphatase domain of polynucleotide kinase, is a third member of this group of redundant 3′ processing enzymes. Unlike Apn1 and Apn2, Tpp1 is specific for the removal of 3′ phosphates at strand breaks and does not possess more general 3′ phosphodiesterase, exonuclease, or AP endonuclease activities. Deletion ofTPP1 in an apn1 apn2 mutant background dramatically increased the sensitivity of the double mutant to DNA damage caused by H2O2 and bleomycin but not to damage caused by methyl methanesulfonate. The triple mutant was also deficient in the repair of 3′ phosphate lesions left by Tdp1-mediated cleavage of camptothecin-stabilized Top1-DNA covalent complexes. Finally, the tpp1 apn1 apn2 triple mutation displayed synthetic lethality in combination with rad52, possibly implicating postreplication repair in the removal of unrepaired 3′-terminal lesions resulting from endogenous damage. Taken together, these results demonstrate a clear role for the lesion-specific enzyme, Tpp1, in the repair of a subset of DNA strand breaks.

Sign in / Sign up

Export Citation Format

Share Document