Biocompatibility assessment of single-walled carbon nanotubes using Saccharomyces cerevisiae as a model organism

以酿酒酵母为模式生物,对单壁碳纳米管进行生物相容性评价

阅读:1

Abstract

BACKGROUND: Single-walled carbon nanotubes (SWCNTs) have many potential applications in various fields. Especially, the unique physicochemical properties make them as the prime candidates for applications in biomedical fields. However, biocompatibility of SWCNTs has been a major concern for their applications. In the study, biocompatibility of oxidized SWCNTs (O-SWCNTs) was assessed using Saccharomyces cerevisiae (S. cerevisiae) as a model organism. RESULTS: Cell proliferation and viability were significantly changed after exposure to O-SWCNTs (188.2 and 376.4 mg/L) for 24 h. O-SWCNTs were internalized in cells and distributed in cytoplasm, vesicles, lysosomes and cell nucleus. The average O-SWCNTs contents in S. cerevisiae were ranged from 0.18 to 4.82 mg/g during the exposure from 0 to 24 h, and the maximum content was reached at 18 h after exposure. Both penetration and endocytosis were involved in the internalization of O-SWCNTs in S. cerevisiae, and endocytosis was the main pathway. Cellular structures and morphology were changed after exposure to O-SWCNTs, such as undulating appearance at the membrane, shrinking of the cytosol, increased numbers of lipid droplets and disruption of vacuoles. ROS and antioxidant enzymes activities were observably changed following exposure. For the treatment at 376.4 mg/L, 20.8% of the total cells was undergone apoptosis. Decrease of mitochondrial transmembrane potential and leakage of cytochrome c from mitochondria were observed after exposure. Moreover, expression levels of apoptosis-related genes were significantly increased. CONCLUSIONS: O-SWCNTs can internalize in S. cerevisiae cells via direct penetration and endocytosis, and distribute in cytoplasm, vesicles, lysosomes and cell nucleus. Besides, O-SWCNTs (188.2 and 376.4 mg/L) can induce apoptosis in S. cerevisiae cells, and oxidative stress is involved in activation of the mitochondria-dependent apoptotic pathway.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。