@misc{Ozawa_Takayuki_Age-related_1996,
 author={Ozawa, Takayuki},
 volume={35},
 number={4},
 copyright={Creative Commons Attribution BY-SA 4.0 license},
 journal={Biotechnologia, vol.35, 4 (1996)-.},
 howpublished={online},
 year={1996},
 publisher={Committee on Biotechnology PAS},
 publisher={Institute of Bioorganic Chemistry PAS},
 language={pol},
 abstract={In normal human hearts, a progressive age-related fragmentation of mitochondrial (mt) DNAinto various-sized deleted (A) mtDNA up to 358 types was documented by a novel total-detectionsystem for deletions. The AmtDNA lacking replication origin(s), minicircles, accumulated up to280 types out of the 358, suggesting a yet unknown replication mechanism in human. Wild-typemtDNA decreased linearly down to 11% of the total with age negatively correlated with AmtDNAand oxidized nucleoside, 8-hydroxy-deoxyguanosine. A remarkable mirror image observed inAmtDNA size distribution as well implies that random hydroxyl-radical attacks resulted in doublestrand break and rejoining of mtDNA as a preferable mechanism to form various AmtDNA ofclosed circular duplex. In the patients with mitochondrial cardiomyopathy, similar fragmentationand oxidative damage in mtDNA was documented at their age 7 to 19 equivalent to the normalsubjects of age over 80. Exposure of a cultured cell line under oxygen stress, 95% oxygen, coldmimic these changes in mtDNA* within 3 days leading an apoptotic cell death, whereas mtDNAlacking cells are relatively immune. These facts support the ‘redox mechanism of ageing’.},
 title={Age-related Fragmentation of Mitochondrial DNA Associated with Oxygen Damage},
 type={Text},
 URL={http://rcin.org.pl/Content/146571/PDF/POZN271_182249_biotechnologia-1996-no4-ozawa.pdf},
 keywords={biotechnology},
}