Cerium and Yttrium Oxide Nanoparticles Against Lead-Induced Oxidative Stress and Apoptosis in Rat Hippocampus

Abstract

Due to numerous industrial applications, lead has caused widespread pollution in the environment; it seems that the central nervous system (CNS) is the main target for lead in the human body. Oxidative stress and programmed cell death in the CNS have been assumed as two mechanisms related to neurotoxicity of lead. Cerium oxide (CeO2) and yttrium oxide (Y2O3) nanoparticles have recently shown antioxidant effects, particularly when used together, through scavenging the amount of reactive oxygen species (ROS) required for cell apoptosis. We looked into the neuroprotective effects of the combinations of these nanoparticles against acute lead-induced neurotoxicity in rat hippocampus. We used five groups in this study: control, lead, CeO2 nanoparticles + lead, Y2O3 nanoparticles + lead, and CeO2 and Y2O3 nanoparticles + lead. Nanoparticles of CeO2 (1000 mg/kg) and Y2O3 (230 mg/kg) were administered intraperitoneally during 2 days prior to intraperitoneal injection of the lead (25 mg/kg for 3 days). At the end of the treatments, oxidative stress markers, antioxidant enzymes activity, and apoptosis indexes were investigated. The results demonstrated that pretreatments with CeO2 and/or Y2O3 nanoparticles recovered lead-caused oxidative stress markers (ROS, lipid peroxidation, and total thiol molecules) and apoptosis indexes (Bax/Bcl-2 and caspase-3 protein expression). Besides, these nanoparticles reduced the activities of lead-induced superoxide dismutase and catalase as well as the ADP/ATP ratio. Interestingly, the best recovery resulted from the compound of these nanoparticles. Based on these outcomes, it appears that this combination may potentially be beneficial for protection against lead-caused acute toxicity in the brain through improving the oxidative stress-mediated programmed cell death pathway.

Curcumin inhibits cell proliferation and promotes apoptosis of laryngeal cancer cells through Bcl-2 and PI3K/Akt, and by upregulating miR-15a

“…Apoptosis of tumor cells is a complex process involving the regulation of numerous genes, including members of the Bcl-2 family, which are among the most important members as they are able to inhibit the apoptosis of cells (19). Bcl-2 and Bcl-extra large are able to inhibit apoptosis of cells, whereas Bcl-2-like protein (Bax) and Bcl-2 homologous antagonist/killer promote apoptosis, and alterations in expression of these genes affects the apoptosis of wild-type cells and the apoptosis of tumor cells (20).…”

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

“…Another interesting work by Estevez et al showed how cerium oxide nanoparticles are able to reduce cell death levels up to 50% in an ex vivo model of ischemia based on mouse hippocampal brain slices . In vivo studies have demonstrated that nanoceria could be used as a protective agent against several forms of neuronal damage, including cerebral ischemia/reperfusion injury, lead‐induced hippocampal damage, diabetic neurophaty, and cognitive impairments caused by hypoxia . Yan et al developed a nanozyme based on Pt/CeO 2 with efficient catalytic activity for the treatment of neurotrauma, and in vivo studies demonstrated that this material can improve the healing and reduce neuroinflammation .…”

“…Yttrium oxide nanoparticles (Y 2 O 3 ) protective antioxidant effects were reported in HT‐22 mouse hippocampal neuronal cells, in a rat model of lead‐induced neuronal damage, and in an in vivo model of photo degeneration. However, Y 2 O 3 ability to ameliorate neurodegenerative disorders in animal models still needs to be tested …”

Toxicity and Protective Effects of Cerium Oxide Nanoparticles (Nanoceria) Depending on Their Preparation Method, Particle Size, Cell Type, and Exposure Route

“…[20] This leads to the protection of eukaryotic cells against oxidative stress, as it was previously reported in many studies. [21,22] Niu et al [23] and Korsvik et al [24] have proposed a mechanism, shown in Equations (2) and (3), by which ceria can scavenge radicals thanks to its redox potential.…”