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静磁场影响钙通量并抑制人胶质母细胞瘤细胞中应激诱导的细胞凋亡。

Static magnetic fields affect calcium fluxes and inhibit stress-induced apoptosis in human glioblastoma cells.

作者信息

Teodori Laura, Göhde Wolfgang, Valente Maria Giovanna, Tagliaferri Fausto, Coletti Dario, Perniconi Barbara, Bergamaschi Antonio, Cerella Claudia, Ghibelli Lina

机构信息

UTS Biotec, Section of Biomedicine and Toxicology, ENEA, Rome, Italy.

出版信息

Cytometry. 2002 Dec 1;49(4):143-9. doi: 10.1002/cyto.10172.

Abstract

BACKGROUND

Epidemiologic data revealed increased brain tumor incidence in workers exposed to magnetic fields (MFs), raising concerns about the possible link between MF exposure and cancer. However, MFs seem to be neither mutagenic nor tumorigenic. The mechanism of their tumorigenic effect has not been elucidated.

METHODS

To evaluate the interference of MFs with physical (heat shock, HS) and chemical (etoposide, VP16) induced apoptoses, respectively, we exposed a human glioblastoma primary culture to 6 mT static MF. We investigated cytosolic Ca(2+) (Ca(2+)) fluxes and extent of apoptosis as key endpoints. The effect of MFs on HS- and VP16-induced apoptoses in primary glioblastoma cultures from four patients was also tested.

RESULTS

Static MFs increased the Ca(2+) from a basal value of 124 +/- 4 nM to 233 +/- 43 nM (P < 0.05). MF exposure dramatically reduced the extent of HS- and VP16-induced apoptoses in all four glioblastoma primary cultures analyzed by 56% (range, 28-87%) and 44% (range, 38-48%), respectively. However, MF alone did not exert any apoptogenic activity. Differences were observed across the four cultures with regard to apoptotic induction by HS and VP16 and to MF apoptotic reduction, with an individual variability with regard to apoptotic sensitivity.

CONCLUSION

The ability of static MFs to reduce the extent of damage-induced apoptosis in glioblastoma cells might allow the survival of damaged and possibly mutated cells.

摘要

背景

流行病学数据显示,暴露于磁场(MFs)的工人脑肿瘤发病率增加,这引发了人们对MF暴露与癌症之间可能联系的担忧。然而,MFs似乎既不具有致突变性也不具有致癌性。其致癌作用的机制尚未阐明。

方法

为了分别评估MFs对物理(热休克,HS)和化学(依托泊苷,VP16)诱导的凋亡的干扰,我们将人胶质母细胞瘤原代培养物暴露于6 mT的静态MF。我们研究了胞质Ca(2+)(Ca(2+))通量和凋亡程度作为关键终点。还测试了MFs对来自四名患者的原发性胶质母细胞瘤培养物中HS和VP16诱导的凋亡的影响。

结果

静态MFs使Ca(2+)从基础值124±4 nM增加到233±43 nM(P < 0.05)。在所有分析的四种胶质母细胞瘤原代培养物中,MF暴露分别使HS和VP16诱导的凋亡程度显著降低56%(范围为28 - 87%)和44%(范围为38 - 48%)。然而,单独的MFs没有发挥任何促凋亡活性。在四种培养物中,关于HS和VP16诱导的凋亡以及MF诱导的凋亡减少存在差异,在凋亡敏感性方面存在个体差异。

结论

静态MFs降低胶质母细胞瘤细胞中损伤诱导凋亡程度的能力可能使受损且可能发生突变的细胞存活。

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