Cerium oxide nanoparticles with antioxidant properties ameliorate strength and prolong life in mouse model of amyotrophic lateral sclerosis

Antioxidants and Nanotechnology: Promises and Limits of Potentially Disruptive Approaches in the Treatment of Central Nervous System Diseases

“…Interestingly, the authors showed that nanoceria had beneficial effects when administrated both in a preventative and in a therapeutic regimen, suggesting that they might have both protective and therapeutic effects . The same group tested nanoceria in a murine model of ALS showing that the administration of cerium oxide nanoparticles could prevent muscle loss and increase the life expectancy of the animals . Also Eitan et al obtained good results using in vivo model of MS, showing that a combined treatment with lenalidomide and nanoceria could reduce the disease symptoms, white matter damage, and inflammatory response in EAE animals .…”

Variable in Vivo and in Vitro Biological Effects of Cerium Oxide Nanoparticle Formulations

“…Though the toxicological effects of accidental and occupational CeNP exposure have been investigated, CeNPs have increasingly been applied to disease models, particularly those involving oxidative stress (Heckman et al, 2013;Bailey et al, 2016;DeCoteau et al, 2016;Kwon et al, 2016;Naz et al, 2017). The administration of CeNPs has recently been shown to be efficacious in models of traumatic brain injury (Bailey et al, 2016), amyotrophic lateral sclerosis (ALS) (DeCoteau et al, 2016), radiation-induced lung damage (Xu et al, 2016), chronic liver (Oró et al, 2016) or kidney injury (Manne et al, 2015a), peritonitis (Manne et al, 2015b), and obesity (Rocca et al, 2015).…”

“…Though the toxicological effects of accidental and occupational CeNP exposure have been investigated, CeNPs have increasingly been applied to disease models, particularly those involving oxidative stress (Heckman et al, 2013;Bailey et al, 2016;DeCoteau et al, 2016;Kwon et al, 2016;Naz et al, 2017). The administration of CeNPs has recently been shown to be efficacious in models of traumatic brain injury (Bailey et al, 2016), amyotrophic lateral sclerosis (ALS) (DeCoteau et al, 2016), radiation-induced lung damage (Xu et al, 2016), chronic liver (Oró et al, 2016) or kidney injury (Manne et al, 2015a), peritonitis (Manne et al, 2015b), and obesity (Rocca et al, 2015). Though it is tempting to extrapolate the applicability of these results to all CeNPs, even within just these few studies, the particles utilized range from 3-80 nm in size, exhibited variable amounts of aggregation, and were delivered at doses ranging from 0.0007 mg/kg (Xu et al, 2016) to 20 mg/kg (DeCoteau et al, 2016) for mice and 0.05 mg/kg (Bailey et al, 2016) to 0.5 mg/kg (Rocca et al, 2015) for rats.…”

“…The administration of CeNPs has recently been shown to be efficacious in models of traumatic brain injury (Bailey et al, 2016), amyotrophic lateral sclerosis (ALS) (DeCoteau et al, 2016), radiation-induced lung damage (Xu et al, 2016), chronic liver (Oró et al, 2016) or kidney injury (Manne et al, 2015a), peritonitis (Manne et al, 2015b), and obesity (Rocca et al, 2015). Though it is tempting to extrapolate the applicability of these results to all CeNPs, even within just these few studies, the particles utilized range from 3-80 nm in size, exhibited variable amounts of aggregation, and were delivered at doses ranging from 0.0007 mg/kg (Xu et al, 2016) to 20 mg/kg (DeCoteau et al, 2016) for mice and 0.05 mg/kg (Bailey et al, 2016) to 0.5 mg/kg (Rocca et al, 2015) for rats. Thus, while different formulations of CeNPs have exhibited antioxidant activity, parallel investigation of the catalytic activity and biological efficacy of CeNPs would strengthen our understanding of how unique characteristics of CeNPs influence their function.…”

“…These CeNPs exhibit catalase and SOD-like activity in vitro, enabling the reduction of ROS levels in murine hippocampal brain slices exposed ex vivo to ischemic conditions (Estevez et al, 2019). Further, the CeNPs oppose peroxide or ischemia induced shifts in the oxidation-reduction potential of brain tissue (DeCoteau et al, 2016). This antioxidant activity translates to in vivo efficacy in oxidative-stress mediated murine models of multiple sclerosis [experimental autoimmune encephalomyelitis (EAE)] (Heckman et al, 2013) and ALS (DeCoteau et al, 2016).…”