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首页> 外文期刊>Archives of Toxicology >Different effects of inorganic and dimethylated arsenic compounds on cell morphology, cytoskeletal organization, and DNA synthesis in cultured Chinese hamster V79 cells.
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Different effects of inorganic and dimethylated arsenic compounds on cell morphology, cytoskeletal organization, and DNA synthesis in cultured Chinese hamster V79 cells.

机译：无机和二甲基化砷化合物对中国仓鼠V79细胞的细胞形态，细胞骨架组织和DNA合成的不同影响。

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摘要

Changes in cytoskeletal organization of cultured V79 cells exposed to arsenite and dimethylarsinic acid (DMAA), a methylated derivative of inorganic arsenics, and related changes, such as mitotic arrest and induction of multinucleated cells, were investigated in comparison with their effects on DNA synthesis. DMAA caused mitotic arrest and induction of multinucleated cells with a delay of 12 h relative to the mitotic arrest. By contrast, arsenite at equitoxic concentrations to DMAA was less effective than DMAA in causing mitotic arrest and in inducing multinucleated cells. Post-mitotic incubation of cells arrested in metaphase by 6 h incubation with 10 mM DMAA showed that the incidence of multinucleated cells increased conversely with a rapid decrease in metaphase cells. This suggests that metaphase-arrested cells can escape from metaphase, resulting in the appearance of multinucleated cells. The mitotic arrest caused by DMAA was accompanied by disruption of the microtubule network. By contrast, both arsenite and DMAA did not cause disorganization of actin stress fibers even when incubated at concentrations that caused a marked retardation of cell growth. Cells exposed to arsenite for 6 h showed marked inhibition of DNA synthesis, whereas inhibition by DMAA was not observed. When incubation was prolonged by 18 h, the arsenite-induced inhibition of DNA synthesis was mitigated. By contrast, inhibition of DNA synthesis by DMAA occurred in parallel with an increase in the population of mitotic cells. These results suggest that DMAA caused growth retardation and morphological changes via disruption of the microtubule network, and that arsenite-induced retardation of cell growth and inhibition of DNA synthesis were not attributable to the cytoskeletal changes.
机译：比较了它们对DNA合成的影响，研究了暴露于亚砷酸和二甲基亚砷酸（DMAA）（一种无机砷的甲基化衍生物）的培养V79细胞的细胞骨架组织变化以及相关变化，例如有丝分裂阻滞和多核细胞的诱导。 DMAA导致有丝分裂阻滞和多核细胞的诱导，相对于有丝分裂阻滞延迟了12 h。相比之下，亚砷酸盐对DMAA的同等毒性在导致有丝分裂停滞和诱导多核细胞方面不如DMAA有效。通过与10 mM DMAA孵育6 h而在中期停滞的细胞进行有丝分裂后孵育表明，多核细胞的发生率反而增加，而中期细胞迅速减少。这表明停滞在中期的细胞可以从中期逃脱，从而导致出现多核细胞。 DMAA引起的有丝分裂阻滞伴随着微管网络的破坏。相比之下，亚砷酸盐和DMAA都不会引起肌动蛋白应激纤维的紊乱，即使在导致细胞生长显着延迟的浓度下孵育也是如此。暴露于亚砷酸盐6 h的细胞显示出明显的DNA合成抑制作用，而未观察到DMAA抑制作用。当孵育时间延长18 h时，砷诱导的DNA合成抑制作用减弱。相比之下，DMAA对DNA合成的抑制与有丝分裂细胞群体的增加同时发生。这些结果表明，DMAA通过破坏微管网络而导致生长迟缓和形态变化，而砷诱导的细胞生长迟缓和DNA合成抑制与细胞骨架的变化无关。

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