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Introduction:Copper oxide nanoparticles (CuO-NPs) are widely used as feed additives for livestock and poultry and implicated in many biomedical applications; however, overload of copper NPs induces various toxicological changes and dysfunction of animal's organs. Thus, this study was designed to evaluate the comparative toxicological effects of biologically and chemically synthesized CuO-NPs on mice. Methods: Transmission electron microscopy (TEM), X-ray diffraction (XRD) and Fouriertransform infrared spectroscopy (FT-IR) were used to characterize the sizes, shapes and functional groups of CuO-NPs. Forty-five mice were randomly allocated into three groups. Control group received distilled water. The second group was administered a single dose of biologically synthesized CuO-NPs (500 mg/kg bw) orally. The third group was administered a single dose of chemically synthesized CuO-NPs (500 mg/kg bw) orally. Results: TEM revealed that biologically synthesized NPs were spherical in shape, whereas chemically synthesized NPs were spherical or elongated in shape. XRD showed that the size of biologically synthesized NPs ranged from 4.14 to 12.82 nm and that of chemically synthesized NPs ranged from 4.06 to 26.82 nm. FT-IR spectroscopy indicated that the peaks appeared between 779 cm −1 and 425 cm −1 in biologically synthesized NPs and between 858 cm −1 and 524 cm −1 in chemically synthesized NPs were for Cu-O nanostructure. Four mice died due to administration of biologically synthesized CuO-NPs. Both biologically and chemically synthesized CuO-NPs induced leukocytosis, elevated serum activities of alanine aminotransferase and aspartate aminotransferase and serum levels of urea and creatinine and increased P53 mRNA and caspase-3 protein expressions in hepatic tissues. Moreover, CuO-NPs induced degenerative and necrotized changes in hepatic, renal and splenic tissues. Biochemical, apoptotic and pathological changes were more serious in mice administered with biologically synthesized CuO-NPs. Conclusion: This study indicated that a high dose of biologically and chemically synthesized CuO-NPs induced adverse effects on hepatic, renal and splenic tissues. At the same dose level, the biologically synthesized CuO-NPs evoked more potent toxic effects than the chemically synthesized CuO-NPs.

This study evaluated the ameliorative impact of Nigella sativa oil (NSO) on emamectin benzoate (EMB) neurotoxicity. Thirty-five male rats were randomly allocated into 5 groups (n = 7). G1 (control): received distilled water; G2: received NSO (3 ml. Kg À1 B.W.) for 6 weeks; G3: received EMB (9 mg kg À1 B.W.) for 6 weeks; G4: was cotreated with NSO and EMB for 6 weeks; G5: was treated with EMB for 4 weeks then, received NSO for 2 weeks. All treatments were given orally every other day.EMB increased serum urea, creatinine levels; brain dopamine, serotonin, malondialdehyde levels; brain expression levels of caspase 3 and TNF-α. While, it decreased serum total protein, albumin, brain GABA, AChE, GSH-Px, CAT, and SOD levels. Histopathological findings revealed hemorrhage, congestion, severe degeneration, and edema of the brain tissues. NSO reversed the EMB-induced biochemical and histopathological alterations. This NSO effect is mostly due to its antioxidant, antiinflammatory, and antiapoptotic activities. These findings suggest NSO as a potential protective and therapeutic agent for EMB-induced neurotoxicity.

The present trial was designed to assess the effect of phytase, multi-strain probiotic, Saccharomyces cerevisiae, and fumaric acid on performance, nutrient digestibility, bone physical parameters and mineralization, blood constituents, bone and gut histomorphology, and duodenal phosphorus transporter genes of broiler chickens fed a decreased non-phytate phosphorus (nPP) diet for 5 weeks. A total of 480 broiler chickens were allotted to six dietary groups and eight replicates each: (1) positive control diet with recommended levels of nPP (PC; 0.48, 0.44, and 0.41% in the three feeding phases); (2) negative control diet with a decreased dietary nPP (NC; 0.28, 0.24, and 0.21% in the three feeding phases); (3) NC + 600 FTU/kg phytase (PHY); (4) NC + 0.05% multi-strain probiotic (PRO); (5) NC + 0.2% Saccharomyces cerevisiae (SC); and (6) NC + 0.2% fumaric acid. Growth performance data were recorded weekly, and blood sampling was performed at days 21 and 35 of age. Bone quality traits, gut and tibia histology, nutrient digestibility, and intestinal gene expression analyses were conducted at the end of the trial (35 days of age). Final body weight and total gain at day 35 of age of the broiler chickens fed with the PHY, PRO, and SC diets were greater (p < 0.01) than in NC, where broilers fed with the PRO and PHY diets had higher values and were similar to that of PC. There was a non-significant variation in the cumulative feed intake among the treatment groups. The PHY and PRO groups had better FCR than the PC group (p < 0.05), and FA and SC had an FCR equivalent to that of PC. The PHY and PRO broilers had greater dressing % than the NC group (p < 0.05) and even better than PC. The PHY, PRO, SC, and FA broilers had higher relative weights of spleen and bursa of Fabricius (p < 0.01) than NC. In comparison to NC, the PHY, PRO, and SC groups improved (p < 0.05) CP, CF, Ca, and P digestibility. Greater tibia breaking strength of the low nPP-supplemented groups was shown to be associated with higher tibia ash, Ca, and P concentrations (p < 0.01) and increased (p < 0.001) tibia cortical area thickness. At days 21 and 35 of age, the dietary supplements to low nPP diets reduced (p < 0.05) serum total cholesterol, triglyceride, triiodothyronine, thyroxine, glucose, and alkaline phosphatase levels, while serum Ca and P concentrations were improved (p < 0.05) compared to NC. All supplements led to enhancement (p < 0.01) in villi height and width and villi absorptive surface area when compared with NC and were even comparable to that of PC. The mRNA expression of NaP-IIb was up-regulated (p < 0.001) in the duodenum of PRO and FA broilers at day 35 of age compared with NC, and their expression levels were similar to that of PC, indicating greater P availability. It is concluded that dietary supplementation of PHY, PRO, SC, and FA to a low nPP diet was advantageous and mitigated the negative impacts of P reduction on the growth performance, health, nutrient digestibility, and bone quality of broilers.

This study was performed to evaluate anti-obesity potential of Commiphora myrrha resin ethanolic extract (CME) with the respect to expression of leptin, adiponectin and uncoupling protein 1 (UCP1) in rats. Control rats fed basal diet. Second group fed basal diet and administered CME (500 mg/kg bw) orally for 14 weeks. Third group fed high fat diet (HFD) for 14 weeks. Fourth group fed HFD and administered CME as second group. Fifth group fed HFD for 8 weeks then fed basal diet and administered CME as third group for another 6 weeks. Phytochemical analysis of CME identified the presence of germacrene B, 1,4-benzoquinone, benzofuran, hexadecanoic acid, 9,12-octadecnoic acid methyl ester, reynosin, 11, 14-eicosadienoic acid, isochiapin B, bisabolene epixod, elemene and 1-heptatriacotanol. High fat diet significantly increased food intake, body weight, hyperglycemia, serum levels of total cholesterol, triacylglycerol, low density lipoprotein and ketone bodies, AST and AST activities, concentration of malondialdehyde and histopathological changes in hepatic tissues. However, it significantly reduced serum levels of high density lipoprotein, leptin and adiponectin, activity of hepatic glutathione reductase (GR) and brown adipose tissue UCP1 protein expression. In contrast, CME ameliorated HFD increased body weight, hyperglycemia, dyslipidemia, ketonemia, hepatic tissues lipid peroxidation, restored hepatic tissue architecture and enhanced protein expression of leptin, adiponectin and UCP1 and activity of hepatic GR. This study indicated that CME ameliorated HFD induced hyperglycemia and dyslipidemia through normalization of HFD reduced leptin, adiponectin and UCP1 proteins production and antioxidant activity.