RESUMO
Background: Nanotechnology has shown a remarkable progress nevertheless, there is a growing concern about probable neurotoxic and neurodegenerative effects due to NPs exposure. Various toxicological and epidemiological studies reported that the brain is a main target for ultrafine particles. Brain inflammation is considered as a possible mechanism that can participate to neurotoxic and neurodegenerative effects. Whether nanoparticles (NPs) may produce neurotoxicity and promote neurodegenerative is largely unstudied. The present study was done to investigate whether intranasal and intra-peritoneal exposure to cerium oxide nanoparticles (CeO2NPs, nanoceria (NC)) could cause neurotoxicity and neurodegenerative changes in the brain tissue through conducting some behavioral tests, biochemical evaluation, histopathological examinations of brain hippocampus and gene expressions. Method: Fifteen mice were separated into 3 equal groups. In group (I) "control group", mice were received distilled water orally and kept as a control group. Mice in the group (II) "NC I/P group" were injected i.p with cerium oxide nanoparticles at a dose of 40 mg/kg b.wt, twice weekly for 3 weeks. In group (III) "NC I/N group" mice were received nanoceria intranasally (40 mg/kg b.wt), twice weekly for 3 weeks. Results: Exposure to nanceria resulted in oxidative damage in brain tissue, a significant increase in malondialdehyde (MDA) and acetylcholinestrase (AchE) levels, significant decrease in reduced glutathione (GSH) concentration, upregulation in the apoptosis-related genes (c-Jun: c-Jun N-terminal kinases (JNKs), c-Fos: Fos protooncogene, AP-1 transcription factor subunit, c-Myc: c-myelocytomatosis oncogene product or MYC protooncogene, bHLH transcription factor), locomotor and cognitive impairment in mice but the effect was more obvious when nanoceria adminstred intraperitoneally. Conculsion: Nanoceria cause oxidative damage in brain tissue of mice when adminstred nanoceria intraperitoneally more than those received nanoceria intranasal.
RESUMO
Background: Cadmium (Cd) is a highly toxic heavy metal that adversely affects both human and animal health. Chronic cadmium exposure causes serious kidney damage. The current study investigated the protective role of cerium oxide nanoparticles (CeO2NPs) against cadmium chloride (CdCl2)-induced renal injury. Method: One hundred and twenty male albino rats were divided into 6 equal groups. Group (C): considered as control group which was given distilled water orally. Group (NC.1 and NC.5): rats were injected i.p. with nanoceria at a dose of (0.1 and 0.5 mg/kg b.wt), respectively, twice a week for 2 weeks starting at the 15th day of the study. Group (Cd): rats were received CdCl2 orally (10 mg/kg b.wt) daily for 28 days. Groups (Cd + NC.1 and Cd + NC.5): rats were given CdCl2 orally (10 mg/kg b.wt) for 28 days and CeO2NPs by i.p. injection at a dose of (0.1 and 0.5 mg/kg b.wt), respectively, twice a week for 2 weeks started at the 15th day of the experiment. Results: The Cd group exhibited a significant increase in the serum levels of IL-1ß, KIM-1, Cys-C, and ß2-MG, downregulation of the antioxidant initiator genes such as Nrf-2, and up-regulation of apoptosis markers such as nibrin gene (NBN). Urine examination showed a high level of microalbuminuria, abnormal physical, chemical, and microscopical changes in comparison with control groups. Conculsion: Remarkably, posttreatment with CeO2NPs showed significant improvement in kidney histopathological picture and relieved the alterations in kidney biomarkers, inflammatory markers, urine abnormalities, and expressions of different genes as Nrf-2 and NBN.
