Polyamine depletion protects HL-60 cells from 2-deoxy-D-ribose-induced apoptosis.

Monti MG; Ghiaroni S; Pernecco L; Barbieri D; Marverti G; Franceschi C

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Polyamine depletion protects HL-60 cells from 2-deoxy-D-ribose-induced apoptosis.

机译：多胺耗竭可保护HL-60细胞免于2-脱氧-D-核糖诱导的细胞凋亡。

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We investigated the involvement of natural polyamines in HL-60 cell death triggered by exposure to 2-deoxy-D-ribose (dRib). In contrast to previous studies, exogenous polyamines failed to protect HL-60 cells against apoptosis caused by dRib. Moreover, in our experimental conditions, depletion of intracellular levels of putrescine and spermidine by alpha-difluoromethylornithine (DFMO) delayed the onset of apoptosis by at least a day or so. Exogenous polyamines reversed the beneficial effect of DFMO and restored the apoptotic levels observed in dRib-treated cells. We suggested that polyamines, especially putrescine and spermidine, act as facilitating factors in the induction of apoptosis triggered by dRib in HL-60 cells.

机译：我们调查了天然多胺参与2-脱氧-D-核糖（dRib）引发的HL-60细胞死亡的过程。与以前的研究相反，外源多胺未能保护HL-60细胞免受dRib引起的细胞凋亡。此外，在我们的实验条件下，α-二氟甲基鸟氨酸（DFMO）耗尽了胞内腐胺和亚精胺的水平，将细胞凋亡的发生延迟了至少一天左右。外源多胺逆转了DFMO的有益作用，并恢复了在dRib处理的细胞中观察到的凋亡水平。我们建议多胺，尤其是腐胺和亚精胺，在HL-60细胞中由dRib触发的凋亡诱导中起促进作用。

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《Life sciences》 |1998年第9期|共8页
作者
Monti MG; Ghiaroni S; Pernecco L; Barbieri D; Marverti G; Franceschi C;
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正文语种 eng
中图分类生命的起源;生命科学总论;
关键词
Apoptosis; Deoxyribose; Putrescine; Spermidine; Ornithine Decarboxylase; 脱噬作用; 脱氧核糖; 腐胺; 精脒;

机译：Apoptosis;Deoxyribose;Putrescine;Spermidine;Ornithine Decarboxylase;脱噬作用;脱氧核糖;腐胺;精脒;

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专利

1. Polyamine depletion protects HL-60 cells from 2-deoxy-D-ribose-induced apoptosis. [J] . Monti MG, Ghiaroni S, Pernecco L, Life sciences . 1998,第9期

机译：多胺耗竭可保护HL-60细胞免于2-脱氧-D-核糖诱导的细胞凋亡。
2. Wr-1065, the active form of amifostine, protects hl-60 cells but not peripheral blood mononuclear cells from radiation and etoposide-induced apoptosis. [J] . Hatoum GF, Nevaldine B, Bhavsar T, International Journal of Radiation Oncology, Biology, Physics . 2004,第3期

机译：Wr-1065是氨磷汀的活性形式，可保护hl-60细胞而不是外周血单核细胞免受辐射和依托泊苷的诱导凋亡。
3. Kaempferol protects HIT-T15 Pancreatic Beta Cells from 2-deoxy-D-ribose-induced Oxidative Damage [J] . Yun Jung Lee, Kwang Sik Suh, Moon Chan Choi, Phytotherapy research: PTR . 2010,第3期

机译：山emp酚保护HIT-T15胰腺β细胞免受2-脱氧-D-核糖诱导的氧化损伤
4. PHASE I/II TRIAL OF DUAL AGENT POLYAMINE DEPLETION THERAPY FOR FELINE ORAL SQUAMOUS CELL CARCINOMA [C] . Katherine A Skorupski, Thomas OBrien, Mark Burns, Annual conference of the Veterinary Cancer Society . 2008

机译：双药剂多胺耗竭治疗猫鳞状鳞状细胞癌的I / II试验
5. Mutations to Bid cleavage sites protect hepatocytes from death receptor- and cell-mediated apoptosis. [D] . Riddle, Erica Delores. 2006

机译：出价切割位点的突变可保护肝细胞免受死亡受体和细胞介导的细胞凋亡。
6. Changes in polyamine catabolism in HL-60 human promyelogenous leukaemic cells in response to etoposide-induced apoptosis. [O] . G S Lindsay, H M Wallace 1999

机译：响应于依托泊苷诱导的凋亡HL-60人早幼粒白血病细胞中多胺分解代谢的变化。
7. Changes in polyamine catabolism in HL-60 human promyelogenous leukaemic cells in response to etoposide-induced apoptosis. [O] . Lindsay, G S, Wallace, H M 1999

机译：响应于依托泊苷诱导的凋亡，HL-60人早幼粒白血病细胞中多胺分解代谢的变化。

Polyamine depletion protects HL-60 cells from 2-deoxy-D-ribose-induced apoptosis.

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