Abstract
Currently, silver nanoparticles (AgNPs) are frequently used in a wide range of medical and consumer products. Substantial usage of AgNPs is considered to create substantive risks to both the environment and the human health. Since there is increasing evidence that the main mechanism of toxicity of AgNPs relates to oxidative stress, in the current study we investigate oxidative stress-related biochemical parameters in myelin isolated from adult rat brain subjected to a low dose of AgNPs. Animals were exposed for 2 weeks to 0.2 mg/kg b.w. of small (10 nm) AgNPs stabilized in citrate buffer or silver citrate established as a control to compare the effects of particulate and ionic forms of silver. We observe enhanced peroxidation of lipids and decreased concentrations of protein and non-protein –SH groups in myelin membranes. Simultaneously, expression of superoxide dismutase, a free radical scavenger, is increased whereas the process of protein glutathionylation, being a cellular protective mechanism against irreversible oxidation, is found to be inefficient. Results indicate that oxidative stress-induced alterations in myelin membranes may be the cause of ultrastructural disturbances in myelin sheaths.
Highlights
Silver nanoparticles (AgNPs) are extensively used in a wide variety of medical and consumer products due to their strong antimicrobial properties
The anti-glutathione antibody used in the present study revealed complexes which are formed between GSH and myelin proteins
It is important to investigate the mechanisms of AgNP-induced neurotoxicity since these nanoparticles show a tendency to accumulate in brain during the period of exposure (Lee et al 2013)
Summary
Silver nanoparticles (AgNPs) are extensively used in a wide variety of medical and consumer products due to their strong antimicrobial properties. There is a need to investigate adverse effects of AgNPs under conditions of prolonged exposure to environmentally relevant doses since our knowledge of the mechanisms of AgNP-induced toxicity, and neurotoxicity, remains insufficient. The mechanisms of neurotoxic effects of AgNPs, and nanoparticles in general, are still under investigation in context of the high susceptibility of the brain to oxidative stress. A number of in vitro studies on the toxicity of AgNPs in various cellular systems have shown that AgNPs influence the function of mitochondria, perturb cellular respiration, and increase free radical production, leading to oxidative stress and cell death (AshaRani et al 2009; Foldbjerg et al 2009; Piao et al 2011; Ziemińska et al 2014). Animal experimental models have linked oxidative stress to AgNP-induced cytotoxicity (Strużyński et al 2013; Wu and Neurotox Res (2019) 35:495–504
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
