Lack of correlation between apoptosis and DNA single-strand breaks in X-irradiated human peripheral blood mononuclear cells in the course of ageing

被引:6
作者
Chauvin, C
Heidenreich, E
Elmendorff-Dreikorn, K
Slor, H
Kutzner, J
Batel, R
Schröder, HC
机构
[1] Johannes Gutenberg Univ Mainz, Inst Physiol Chem, Angew Mol Biol Abt, D-55099 Mainz, Germany
[2] Univ Mainz Klinikum, Klin & Poliklin Radiol, D-55101 Mainz, Germany
[3] Tel Aviv Univ, Sackler Sch Med, Dept Human Genet, Tel Aviv, Israel
[4] Rudjer Boskovic Inst, Ctr Marine Res, Lab Marine Mol Toxicol, Rovinj 52210, Croatia
关键词
apoptosis; DNA single-strand breaks; DNA unwinding; X-irradiation; ageing;
D O I
10.1016/S0047-6374(98)00110-9
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
The dependence on age of both the basal and the X-radiation-induced levels of apoptosis was examined in human peripheral blood mononuclear cells (PBMC). In the same samples, the base value and the extent of induced DNA single-strand breaks were determined, using a sensitive and fast microplate assay. PBMC were isolated from blood of donors of various age groups (20-30, 40-60 and > 70 years of age) and X-irradiated ex vivo using a 6 MV linear accelerator to give a total exposure of 4 Gy. The mean basal levels of apoptosis in PBMC from donors in the 40-60 year age group and the > 70 year age group were found to be only slightly higher (by 20-10%) compared to that of the 20-30 year age group, whereas the extent of DNA damage strongly and significantly (P < 0.01) increased with age by up to 2-fold. In contrast to the extent of induced DNA damage, which steadily increased in the course of ageing by up to 1.8-fold, there was only a transient increase in the level of induced apoptosis to 1.5-fold in PBMC from X-irradiated blood (4 Gy photons) from donors aged 40-60 followed by a decrease to 0.9-fold in PBMC from old donors (> 70), compared to age group 20-30. The results show that X-ray-induced apoptosis and DNA damage in PBMC are not correlated during ageing. (C) 1998 Elsevier Science Ireland Ltd. All rights reserved.
引用
收藏
页码:117 / 128
页数:12
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