期刊文献+

口服纳米四氧化三铁和氯化镉对小鼠肝脏的联合毒性 被引量:2

Combined toxicity of Fe3O4 nanoparticles and cadmium chloride in the liver of mice by oral route
下载PDF
导出
摘要 报道了纳米四氧化三铁和氯化镉对小鼠肝脏的联合毒性.在连续7d给小鼠灌胃给药纳米四氧化三铁、氯化镉或二者混合物(纳米四氧化三铁+氯化镉)后,测定了肝脏的脏器系数、组织病理学变化、血清生化参数和氧化应激反应.结果表明,纳米四氧化三铁和氯化镉会竞争性抑制小鼠肝脏对铁和镉的摄取.口服纳米四氧化三铁(50mg/kg体重)没有对小鼠肝脏产生明显的毒性,而口服氯化镉(2.0mg/kg体重)对小鼠肝脏产生显著的氧化应激损伤.同时口服纳米四氧化三铁与氯化镉后,纳米四氧化三铁能够显著降低由氯化镉诱导的肝的氧化应激,从而显著减少氯化镉对肝脏的损伤.同时口服纳米四氧化三铁与氯化镉后,纳米四氧化三铁不仅能显著减少镉在肝脏的积累,而且能抑制由镉引起的肝脏中铁的缺乏,这是纳米四氧化三铁保护肝脏免遭氯化镉诱导氧化损伤的两个关键作用机制.纳米四氧化三铁可以作为镉中毒患者完美的磁共振造影剂和药物载体,因为它在发挥磁共振造影剂和药物载体功能的同时,可以减少镉的毒性. The combined toxicity of Fe3O4 nanoparticles(nano-Fe3O4)and CdCl2 in the liver of mice was reported.The organ coefficient,histopathological changes,serum biochemical parameters and oxidative stress responses were determined in the liver of mice after oral administration of nano-Fe3O4 and/or CdCl2 for 7 d.The results show that nano-Fe3O4 and CdCl2 mutually competitively inhibit Fe and Cd uptake in the liver.Oral nano-Fe3O4(50 mg/kg BW)does not induce obvious injury in mice.In contrast,oral CdCl2(2.0 mg/kg BW)causes signigicant oxidative damage in the liver.Co-administration of nano-Fe3O4 with CdCl2 significantly attenuates CdCl2-induced damage in the liver through reduction of oxidative stress.The inhibition of Cd-induced deprivation of tissue Fe and decrease in Cd accumulation after co-administration of nano-Fe3O4 with CdCl2 might play two key roles in the protective effect of nano-Fe3O4 on CdCl2-induced oxidative damage.Nano-Fe3O4 may be used as a perfect MRI contrast agent and drug carrier for patients with Cd poisoning,since it not only acts as an MRI contrast agent or drug carrier,but also simultaneously attenuates Cd-induced toxicity.
作者 龚家春 张燕 桂宗祥 胡婷婷 王晓琴 王子怡 徐小龙 GONG Jiachun;ZHANG Yan;GUI Zongxiang;HU Tingting;WANG Xiaoqin;WANG Ziyi;XU Xiaolong(Department of Chemistry,University of Science and Technology of China,Hefei,230026,China)
出处 《中国科学技术大学学报》 CAS CSCD 北大核心 2019年第6期431-438,共8页 JUSTC
关键词 纳米四氧化三铁 联合毒性 nano-Fe3O4 Cd joint toxicity liver
  • 相关文献

同被引文献8

引证文献2

二级引证文献7

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部