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量子点在细胞内环境中诱导热休克相关的细胞毒性。

Quantum dots induce heat shock-related cytotoxicity at intracellular environment.

作者信息

Migita Satoshi, Moquin Alexandre, Fujishiro Hitomi, Himeno Seiichiro, Maysinger Dusica, Winnik Françoise M, Taniguchi Akiyoshi

机构信息

Biomaterials Unit, National Institute for Materials Science, 1-1 Namiki, Tsukuba, Ibaraki, 305-0044, Japan,

出版信息

In Vitro Cell Dev Biol Anim. 2014 Apr;50(4):367-72. doi: 10.1007/s11626-013-9693-2. Epub 2013 Oct 3.

Abstract

Quantum dots (QDs) are semiconductor nanocrystals with unique optical properties. Different proteins or polymers are commonly bound to their surfaces to improve biocompatibility. However, such surface modifications may not provide sufficient protection from cytotoxicity due to photodegradation and oxidative degradation. In this study, the cytotoxic effects of QDs, CdTe, and CdSe/ZnS were investigated using cadmium-resistant cells. CdTe QDs significantly reduced cell viability, whereas, CdSe/ZnS treatment did not markedly decrease the cell number. CdTe QDs were cytotoxic in cadmium-resistant cells suggesting that internalized QDs degraded and cadmium ions contributed to the cytotoxic effects. CdTe QDs were consistently more cytotoxic than CdSe/ZnS QDs, but both QDs as well as cadmium ions activated heat shock protein 70B' promoter. QDs themselves are likely to contribute to HSP70B' promoter activation in cadmium-resistant cells, because CdSe/ZnS QDs do not release sufficient cadmium to activate this promoter.

摘要

量子点(QDs)是具有独特光学性质的半导体纳米晶体。不同的蛋白质或聚合物通常结合在其表面以提高生物相容性。然而,由于光降解和氧化降解,这种表面修饰可能无法提供足够的细胞毒性保护。在本研究中,使用耐镉细胞研究了量子点、碲化镉(CdTe)和硒化镉/硫化锌(CdSe/ZnS)的细胞毒性作用。碲化镉量子点显著降低细胞活力,而硒化镉/硫化锌处理并未明显减少细胞数量。碲化镉量子点在耐镉细胞中具有细胞毒性,表明内化的量子点降解且镉离子导致了细胞毒性作用。碲化镉量子点始终比硒化镉/硫化锌量子点具有更强的细胞毒性,但两种量子点以及镉离子均激活了热休克蛋白70B'启动子。量子点本身可能在耐镉细胞中促成了热休克蛋白70B'启动子的激活,因为硒化镉/硫化锌量子点释放的镉不足以激活该启动子。

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