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Cadmium toxicity and its relationship with disturbances in the cytoskeleton, cell cycle and chromosome stability.
Ecotoxicology ( IF 2.4 ) Pub Date : 2019-09-09 , DOI: 10.1007/s10646-019-02096-0
Daniel Pizzaia 1 , Marina Lima Nogueira 1 , Mateus Mondin 1 , Marcia Eugenia Amaral Carvalho 1 , Fernando Angelo Piotto 2 , Millor Fernandes Rosario 3 , Ricardo Antunes Azevedo 1
Affiliation  

This study aimed to investigate the mode of action of cadmium (Cd) toxicity at cell level, especially at early stages of plant exposure. Tomato seedlings were cultivated in growth media containing from 0.1 to 70 µM CdCl2 for 24 h. Mitotic index, chromosome abnormality, DNA integrity and organization of tubulin-based structures were assessed in root cells. As higher the Cd concentration in the growth media, higher was the DNA damage intensity and the occurrence of chromosomal abnormalities that included chromosome lost, bridges, stickiness, C-metaphase and polyploidy. The profile of chromosomal aberrations also varied with elevated Cd concentration, being observed increases in the frequency of chromosome stickiness. The mitotic index was reduced at the lowest Cd concentration, but such reduction was statistically similar to that detected at the highest concentration, suggesting that mitotic depression is a rapid outcome and, at same time, a Cd-induced effect that is limited at the first 24 h of direct root exposure to this metal. Under exposure to 20 µM CdCl2, heterogenous distribution of the spindle fibers, formation of two spindle complexes in both of the cell poles, absence of centrosome center, polarization of the spindle fibers during cell division, and non-uniform tubulin deposition in microtubule and phragmoplast were noticed. The results indicate that the tubulin-dependent components of cytoskeleton are Cd targets, and the sensitivity of tubulin-based structures to Cd exposure depends on cell cycle phase. Moreover, DNA damage intensity and chromosomal abnormality profile can be employed as markers of Cd toxicity level.

中文翻译:

镉毒性及其与细胞骨架,细胞周期和染色体稳定性紊乱的关系。

这项研究旨在研究镉(Cd)毒性在细胞水平上的作用方式,尤其是在植物暴露的早期阶段。将番茄幼苗在含有0.1至70 µM CdCl2的生长培养基中培养24小时。在根细胞中评估了有丝分裂指数,染色体异常,DNA完整性和微管蛋白基结构的组织。随着生长培养基中Cd浓度的升高,DNA损伤强度和染色体异常的发生率也将升高,这些异常包括染色体丢失,桥连,粘性,C中期和多倍性。染色体畸变的轮廓也随镉浓度的升高而变化,观察到染色体粘性的频率增加。在最低的Cd浓度下,有丝分裂指数降低,但这种减少在统计学上与在最高浓度下检测到的减少相似,这表明有丝分裂抑制是快速的结果,同时,Cd诱导的作用在根系直接暴露于该金属的最初24小时内受到限制。在暴露于20 µM CdCl2的情况下,纺锤体纤维的分布不均,在两个细胞极中形成两个纺锤体复合物,不存在中心体中心,纺锤体纤维在细胞分裂过程中发生极化,微管蛋白和原生质体中的微管蛋白沉积不均匀。被注意到。结果表明,细胞骨架的微管蛋白依赖性成分是Cd靶标,基于微管蛋白的结构对Cd暴露的敏感性取决于细胞周期阶段。此外,
更新日期:2019-11-01
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