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-1β, KIM-1, Cys-C, and β2-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.
| Lumpy skin disease (LSD) is an acute, sub-acute and chronic devastating disease of cattle. The current study was performed to determine various alterations in some haemato-biochemical parameters in calves naturally infected with lumpy skin disease virus (LSDV). Two groups of calves were enrolled in the study. The first group included nine Laboratory confirmed LSDV infected calves and the second group included five healthy calves. Laboratory confirmation was conducted by polymerase chain reaction (PCR) flanking the partial RPO30 gene. Blood samples were collected from all calves and subjected to hematological and biochemical analyses. The total mean leukocytic counts, lymphocytes, and monocytes in the LSDV infected calves were significantly higher than those in the control group. In addition, the total protein, total creatine kinase (CK), aspartate aminotransferase (AST), blood urea nitrogen (BUN), creatinine and potassium levels showed significant high values in LSDV infected calves while cholesterol levels were significantly lowered when compared to healthy ones. Serum gamma glutamyl transferase (GGT) activity, serum albumin, globulins and sodium levels did not show significant difference in calves in different groups. Results of both hematology and biochemistry profiles obtained from calves reflect the severe inflammatory process associated with natural LSD infection.
D iclofenac sodium is one of the most commonly used non-steroidal anti-inflammatory drugs (NSAIDs). It is frequently used to treat pain in musculoskeletal injuries, osteoarthritis and rheumatoid (Francio et al., 2017) and used generally in human and veterinary practice (Ramesh et al., 2002). Drug-induced liver injury considered as a major problem and has become a leading cause of acute liver failure and transplantation.The mechanism of DS hepatotoxicity including CYP450 enzyme that oxidizes DS to form reactive metabolites (5-OH and 4-OH DcNa) which oxidizes the benzoquinone imine. Reduced glutathione (GSH) plays an important role in detoxification, conjugation and removing of these metabolites outside the cells. Thus, an elevated dose of DS may lead to GSH depletion which reflected liver injury (Lauer et al., 2009) and inducing hepatocytes apoptosis by the generation of oxidative stress and mitochondrial dysfunction (Gómez-Lechón, et al., 2003). Therefore, many therapeutic agents are used to reverse or arrest cytotoxic action activated by diclofenac.
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