Zhu Hai, Liu Yake, Hong Hongxiang, Wang Wei, Liu Fan
Department of Orthopaedics, Affiliated Hospital of Nantong University, Nantong, Jiangsu Province, China.
Department of Orthopaedics, The Second Affiliated Hospital of Nantong University, Nantong, Jiangsu Province, China.
Biochem Biophys Res Commun. 2017 Apr 29;486(2):357-363. doi: 10.1016/j.bbrc.2017.03.045. Epub 2017 Mar 14.
Recent concerns have emerged surrounding the toxicity that cobalt may represent when used in MOM implants. Owing to corrosion and wear of MOM implants, the subsequent released cobalt nanoparticles (CoNPs) or Co ions (Co) can cause adverse reactions, such as the generation of pseudotumors, extensive necrosis, early osteolysis, and implants failure. The present study confirmed that CoNPs and Co can induce dose- and time-dependent cytotoxicity with increasing reactive oxygen species (ROS) levels. Additionally, using metallothionein (MT), a heavy metal-binding protein, the present study assessed the protective effects of Zn against CoNPs and Co-induced cytotoxicity of RAW 264.7 cells through ROS pathway. Further studies are needed to explore the underlying protective mechanisms in vitro. However, the current findings indicate that the ROS pathway may be a potential target for therapeutic interventions.
最近,人们开始关注钴在金属对金属(MOM)植入物中使用时可能存在的毒性。由于MOM植入物的腐蚀和磨损,随后释放的钴纳米颗粒(CoNP)或钴离子(Co)会引起不良反应,如假肿瘤的产生、广泛坏死、早期骨溶解和植入物失效。本研究证实,CoNP和Co可通过增加活性氧(ROS)水平诱导剂量和时间依赖性细胞毒性。此外,本研究使用金属硫蛋白(MT),一种重金属结合蛋白,通过ROS途径评估了锌对CoNP和Co诱导的RAW 264.7细胞毒性的保护作用。需要进一步的研究来探索体外潜在的保护机制。然而,目前的研究结果表明,ROS途径可能是治疗干预的潜在靶点。