V G Reshma, P V Mohanan
Toxicology Division, Biomedical Technology Wing, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Trivandrum, Kerala, India.
Toxicology Division, Biomedical Technology Wing, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Trivandrum, Kerala, India.
Colloids Surf B Biointerfaces. 2017 Sep 1;157:182-190. doi: 10.1016/j.colsurfb.2017.05.069. Epub 2017 May 31.
Zinc oxide nanoparticles (ZnO NPs) have potential biomedical, industrial and commercial applications. So they constantly come into contact with the body parts during applications. Safety concerns about ZnO NPs are increasing today and yet only few reports are available about their toxicity in kidney cells. It is very essential to analyze the toxicity on kidney because kidney plays a decisive role in nanoparticles excretion. Therefore, the present study focuses on the interaction of ZnO NPs with human embryonic kidney 293 (HEK 293) cells in vitro. The results showed that the cellular viability was much affected by ZnO NPs in a dose and time dependent manner. Oxidative stress increased the formation of reactive oxygen species (ROS), was found to be the prime mechanism of cytotoxicity. Formation of ROS eventually induced loss of mitochondrial membrane potential, lysosomal activity and nuclear condensation, which ultimately leads to apoptosis.
氧化锌纳米颗粒(ZnO NPs)具有潜在的生物医学、工业和商业应用。因此,它们在应用过程中会不断与身体部位接触。如今,人们对ZnO NPs的安全性担忧日益增加,但关于其在肾细胞中的毒性的报道却很少。分析其对肾脏的毒性非常重要,因为肾脏在纳米颗粒排泄中起决定性作用。因此,本研究聚焦于ZnO NPs与人类胚胎肾293(HEK 293)细胞在体外的相互作用。结果表明,细胞活力受到ZnO NPs的显著影响,且呈剂量和时间依赖性。氧化应激增加了活性氧(ROS)的形成,被发现是细胞毒性的主要机制。ROS的形成最终导致线粒体膜电位丧失、溶酶体活性改变和核浓缩,最终导致细胞凋亡。