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氧化应激导致氧化钴纳米颗粒诱导人肝癌细胞的细胞毒性和 DNA 损伤。

Oxidative stress contributes to cobalt oxide nanoparticles-induced cytotoxicity and DNA damage in human hepatocarcinoma cells.

机构信息

Cell and Molecular Laboratory, Department of Zoology, Faculty of Science, King Saud University, Riyadh, Saudi Arabia.

出版信息

Int J Nanomedicine. 2013;8:189-199. doi: 10.2147/IJN.S37924. Epub 2013 Jan 8.

DOI:10.2147/IJN.S37924
PMID:23326189
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3544340/
Abstract

BACKGROUND

Cobalt oxide nanoparticles (Co(3)O(4)NPs) are increasingly recognized for their utility in biological applications, magnetic resonance imaging, and drug delivery. However, little is known about the toxicity of Co(3)O(4)NPs in human cells.

METHODS

We investigated the possible mechanisms of genotoxicity induced by Co(3)O(4)NPs in human hepatocarcinoma (HepG2) cells. Cell viability, reactive oxygen species (ROS), glutathione, thiobarbituric acid reactive substance, apoptosis, and DNA damage were assessed in HepG2 cells after Co(3)O(4)NPs and Co(2+) exposure.

RESULTS

Co(3)O(4)NPs elicited a significant (P < 0.01) reduction in glutathione with a concomitant increase in lipid hydroperoxide, ROS generation, superoxide dismutase, and catalase activity after 24- and 48-hour exposure. Co(3)O(4)NPs had a mild cytotoxic effect in HepG2 cells; however, it induced ROS and oxidative stress, leading to DNA damage, a probable mechanism of genotoxicity. The comet assay showed a statistically significant (P < 0.01) dose- and time-related increase in DNA damage for Co(3)O(4)NPs, whereas Co(2+) induced less change than Co(3)O(4)NPs but significantly more than control.

CONCLUSION

Our results demonstrated that Co(3)O(4)NPs induced cytotoxicity and genotoxicity in HepG2 cells through ROS and oxidative stress.

摘要

背景

氧化钴纳米粒子(Co(3)O(4)NPs)因其在生物应用、磁共振成像和药物输送方面的应用而越来越受到关注。然而,人们对 Co(3)O(4)NPs 在人细胞中的毒性知之甚少。

方法

我们研究了 Co(3)O(4)NPs 在人肝癌(HepG2)细胞中诱导遗传毒性的可能机制。在 Co(3)O(4)NPs 和 Co(2+)暴露后,评估 HepG2 细胞中的细胞活力、活性氧(ROS)、谷胱甘肽、硫代巴比妥酸反应物质、细胞凋亡和 DNA 损伤。

结果

Co(3)O(4)NPs 在 24 小时和 48 小时暴露后,显著(P < 0.01)降低了谷胱甘肽,同时增加了脂质过氧化物、ROS 生成、超氧化物歧化酶和过氧化氢酶活性。Co(3)O(4)NPs 对 HepG2 细胞具有轻度细胞毒性作用;然而,它诱导了 ROS 和氧化应激,导致 DNA 损伤,这可能是遗传毒性的一种机制。彗星试验显示 Co(3)O(4)NPs 与 DNA 损伤呈剂量和时间相关的显著增加(P < 0.01),而 Co(2+) 引起的变化小于 Co(3)O(4)NPs,但明显大于对照。

结论

我们的结果表明,Co(3)O(4)NPs 通过 ROS 和氧化应激诱导 HepG2 细胞的细胞毒性和遗传毒性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a516/3544340/ea0aa77b7a75/ijn-8-189f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a516/3544340/741c99f90489/ijn-8-189f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a516/3544340/7e75c6997d1b/ijn-8-189f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a516/3544340/8c6338159adb/ijn-8-189f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a516/3544340/413f63537c1a/ijn-8-189f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a516/3544340/dae655815519/ijn-8-189f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a516/3544340/cd4bcef968f3/ijn-8-189f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a516/3544340/ea0aa77b7a75/ijn-8-189f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a516/3544340/741c99f90489/ijn-8-189f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a516/3544340/7e75c6997d1b/ijn-8-189f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a516/3544340/8c6338159adb/ijn-8-189f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a516/3544340/413f63537c1a/ijn-8-189f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a516/3544340/dae655815519/ijn-8-189f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a516/3544340/cd4bcef968f3/ijn-8-189f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a516/3544340/ea0aa77b7a75/ijn-8-189f7.jpg

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