CELL INACTIVATION AND CELL-CYCLE INHIBITION AS INDUCED BY EXTREME HYPOXIA - THE POSSIBLE ROLE OF CELL-CYCLE ARREST AS A PROTECTION AGAINST HYPOXIA-INDUCED LETHAL DAMAGE

CELL INACTIVATION AND CELL-CYCLE INHIBITION AS INDUCED BY EXTREME HYPOXIA - THE POSSIBLE ROLE OF CELL-CYCLE ARREST AS A PROTECTION AGAINST HYPOXIA-INDUCED LETHAL DAMAGE
复制标题

DOI:
10.1111/j.1365-2184.1991.tb01144.x
复制
发表时间:
1991-03-01
期刊:
影响因子:
8.5
通讯作者:
PETTERSEN, EO
PETTERSEN, EO
中科院分区:
生物学1区
文献类型:
--
作者:
AMELLEM, O;PETTERSEN, EO

文献摘要

被引文献

相似文献

极度缺氧(< ppm O2)的循环哺乳动物细胞往往会在 DNA 合成前阶段积累。 目前尚不清楚这是否是细胞主动调节的结果。 在本研究中,我们通过有丝分裂选择使细胞在相对较长的时间内(长达 48 小时)处于极度缺氧状态。 我们记录了缺氧期间的细胞周期进展以及细胞失活,具体取决于开始缺氧处理时细胞在细胞周期中的位置。 得出三个主要结论: 1 即使在长期(24 小时)低氧处理期间,G1 晚期的细胞周期停滞也是完全的; 2 早期和中期的细胞在缺氧条件下完全停滞并迅速失活,而晚期、G2 和有丝分裂的细胞能够继续细胞周期进程和分裂; 3 无论细胞在缺氧开始时处于G2、有丝分裂还是早期G1,它们都能够在相对持久的缺氧治疗中存活。 目前的结果支持这样的观点:极度缺氧诱导的 DNA 合成前停滞可能有助于拯救细胞免受严重破坏性影响,如果细胞能够启动 DNA 合成,就会出现这种严重破坏性影响。
Cycling mammalian cells that are rendered extremely hypoxic (< ppm O2) tend to accumulate in a pre-DNA-synthesis stage. It is not clear whether or not this is the result of an active regulation by the cells. In the present study we have rendered cells, synchronized by mitotic selection, extremely hypoxic over a relatively long period of time (up to 48 h). We have recorded cell cycle progression during hypoxia as well as cell inactivation depending on where in the cell cycle the cells were located when the hypoxic treatment was started. Three main conclusions are drawn: 1 the cell cycle arrest in late-G1 is complete even during a long-lasting (24 h) hypoxic treatment; 2 while cells in early- and mid-S are completely arrested and quickly inactivated under hypoxic conditions, cells in late-S, G2 and mitosis are able to continue cell cycle progression and divide; 3 whether the cells are located in G2, mitosis or early-G1 at the onset of hypoxia, they were able to survive relatively long-lasting hypoxic treatment. The present results are in favour of the view that the pre-DNA-synthetic arrest induced by extreme hypoxia may function to rescue the cells from severely damaging effects that would appear if the cells were able to initiate DNA synthesis.