The promotion effect of novel magnetic nanoparticles on atherosclerotic plaque vulnerability in apolipoprotein E mice.

Toxicology

State Key Laboratory of Biobased Material and Green Papermaking, School of bioengineering, Qilu University of Technology, Shandong Academy of Sciences, Jinan, 250353, China; Institute of Developmental Biology, School of Life Science, Shandong University, Jinan, 250100, China. Electronic address:

Published: May 2019

AI Article Synopsis

  • Manufactured magnetic nanoparticles (NPs), specifically FeO-AG NPs, were found to have toxic effects on the cardiovascular system, particularly increasing the vulnerability of atherosclerotic plaques.
  • In laboratory studies, FeO-AG NPs caused apoptosis in human umbilical vein endothelial cells (HUVECs) and promoted plaque vulnerability in mice at low doses (0.5 mg/kg), while higher doses did not have this effect.
  • The toxicity linked to FeO-AG NPs was associated with a significant reduction in nitric oxide (NO) production, which is crucial for maintaining vascular health—indicating that these nanoparticles should be used with caution despite their effectiveness in removing pollutants from water.

Article Abstract

Although manufactured magnetic nanoparticles (NPs) are currently used in many fields, NPs have potential toxicity on cardiovascular system especially atherosclerosis. In our previous study, we prepared novel FeO nanoparticles surface-coated with aminoguanidine (FeO-AG NPs) which could remove acid dyes from aqueous solution efficiently. To understand its biocompatibility to atherosclerotic plaque vulnerability, we investigated the effects of the nanoparticles on human umbilical vein endothelial cells (HUVECs) in vitro and plaque stability in vivo. FeO-AG NPs were taken up by HUVECs and induced HUVEC apoptosis. FeO-AG NP injection remarkably promoted plaque vulnerability at low-dose (0.5 mg/kg) but not high-dose (5.0 mg/kg) in apolipoprotein E (ApoE) mice. Further study indicated that FeO-AG NP-induced atherosclerotic plaque vulnerability was tightly linked to bioactivity of nitric oxide (NO). A significant decrease in NO production was induced which coincided with the inhibition of endothelial nitric oxide synthase (eNOS) activity in serum and endothelium of plaque in ApoE mice injected with low-dose FeO-AG NPs in vivo and HUVECs treated with low-dose FeO-AG NPs in vitro. Thus, the low concentration of FeO-AG NPs presented toxicity to atherosclerosis. Our results indicated that the use of FeO-AG NPs to improve aqueous solution pollution should be cautious due to the potential toxicity.

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Source
http://dx.doi.org/10.1016/j.tox.2019.03.002DOI Listing

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