Chudinova E M, Nadezhdina E S, Ivanov P A
Biofizika. 2010 Sep-Oct;55(5):857-61.
It has been examined whether the destruction of cell microtubules affects the increase in the intracellular hydrogen peroxide concentration caused by sodium arsenite, which induces the formation of stress ribonucleoprotein granules. As expected, sodium arsenite caused a 50% increase in hydrogen peroxide concentration in HeLa cells; on the other hand, another stress granule inducer tert-buthylhydroquinone did not affect the peroxide concentration. The disruption of microtubules by nocodazole or vinblastine also resulted in some increase in the intracellular peroxide concentration,y taxol did not affect it. The combined treatment of cells with and the microtubule stabilization by taxol did not affect it. The combined treatment of cells with arsenite and antimicrotubule drugs caused an additive effect, and the peroxide concentration increased twice or more. Thus, the inhibition of stress granule formation after microtubule disruption cannot be explained by a decrease in peroxide concentration as compared with the affect of arsenite.
已研究细胞微管的破坏是否会影响由亚砷酸钠引起的细胞内过氧化氢浓度的增加,亚砷酸钠会诱导应激核糖核蛋白颗粒的形成。正如预期的那样,亚砷酸钠使HeLa细胞中的过氧化氢浓度增加了50%;另一方面,另一种应激颗粒诱导剂叔丁基对苯二酚并未影响过氧化物浓度。诺考达唑或长春碱对微管的破坏也导致细胞内过氧化物浓度有所增加,但紫杉醇并未产生影响。用紫杉醇对细胞进行联合处理并使其微管稳定也未产生影响。用亚砷酸盐和抗微管药物对细胞进行联合处理产生了累加效应,过氧化物浓度增加了两倍或更多。因此,与亚砷酸盐的作用相比,微管破坏后应激颗粒形成的抑制不能用过氧化物浓度的降低来解释。