In the current study, fennel essential oil was used as an antibiotic alternative compared to gentamycin for enhancing the expression of apoptosis genes and antioxidant enzymes in weaned rabbits as well as meat quality and growth performance. The gene expression of the cell lymphoma 2 (BAX and BCL2), caspase3 (CASP3), and glutathione peroxidase (GPX1) were estimated in the liver tissue using qRT-PCR. A total of 45 Moshtohor weaned male rabbits aged four weeks were randomly allocated to control, T1, and T2 treatment groups; each consisted of 15 weaned male rabbits with five replicates. Rabbits in the T1 and T2 groups were orally supplied with 1 mL fennel oil and 1 mL gentamycin, respectively. Weaned rabbits under different treatments showed increased body weight (BW) at 8 and 12 weeks of age and average daily gain (ADG) at 4–8 and 4–12 weeks of age compared to the control group. Compared to the controls, the weaned rabbits supplemented with fennel oil and gentamycin had lower total cholesterol, triglyceride, and MDA. In addition, villus length, mRNA of BAX, BCL2, Casp3, and GPX were increased in the different treatments compared to the control. Furthermore, the meat of these rabbits was less tender, had a lower aerobic plate count (APC), pH, and was brighter and redder in color than the control. Under the conditions of the present study, the supplementation of weaned Moshtohor rabbits with fennel oil as a natural alternative for gentamycin enhanced feed conversion and daily gain through enhancing villus length and mucus thickness. Additionally, fennel essential oil reduces oxidative stress by increasing the antioxidant enzymes.
Phycocyanin isolated from Anabaena biomass was in-vitro assayed for its antioxidant activity against DPPH (2,2-diphenyl-1-picrylhydrazyl) and ABTS [2,2′-azino-bis(3ethylbenzothiazoline-6-sulfonic acid)] free radical, revealing maximum activities amounting to 77 and 80% at 1,000 µg/ml and SC 50 values about 96 and 111 µg/ ml, respectively. A biological experiment was conducted, involving 40 male Wistar Albino rats, divided into five groups. Group I received only the basal diet as a normal control, while groups II, III, IV, and V were administrated intraperitoneal (IP) injection of a single dose of CCl 4 (50% in corn oil) at 0.5 ml/kg body weight. Subsequently, groups II, III, IV, and V received phycocyanin at 0.0, 25, 50, and 100 mg/kg body weight/day. CCl 4 induced considerable increases (p < .05) in the levels of serum ALT, AST, urea and creatinine, total lipid, and triglycerides coupled with significant reductions (p < .05) in serum antioxidant enzymes and some liver histopathological deformations compared to the negative control (group 1). Administration of Anabaena oryzae phycocyanin can counteract these CCl 4-induced changes. Practical applications Phycocyanin isolated from Anabaena has beneficial effects such as the antioxidant, antibacterial, anticancer, and hepatoprotective effect. Phycocyanin may play a key role in alleviating oxidative stress, artificially induced by carbon tetrachloride in Albino rats, to ultimately determine its capacity to serve as a natural antioxidant for food and health applications.
In this investigation, hepatorenal antioxidant effects of combined oral administration of ammonium metavanadate (AMV; 0.15 mg V/ml) and nickel sulfate (NS; 0.18 mg Ni/ml) in male albino rats over a 21day period have been evaluated. After administration of vanadium, lipid peroxidation (LPO) increased significantly (p < 0.001) in kidney and insignificantly (p > 0.05) in liver, superoxide dismutase (SOD) and glutathione-S-transferase (GST) activities increased significantly in kidney (p < 0.01) and decreased in liver (p < 0.001) whereas glutathione (GSH) content decreased (p < 0.001) in both organs. The exposure to nickel led to a significant decrease (p < 0.001) in SOD, GST activities in liver and GSH content in kidney and a significant (p < 0.001) increase in the hepatic MDA content and renal SOD activity. When the metals were administered in combination, the elevation of lipid peroxidation did not potentiate. However, the inhibition in hepatic SOD was augmented. In the other hand, the combined metals treatment slightly improved the decreased hepatic GST activity and induced the hepatorenal content of GSH. Signs of toxicity were observed following treatment with vanadium, not nickel nor combined vanadium and nickel. A reduction in cellular enzymatic (SOD) and non-enzymatic (GSH) antioxidants is clearly indicative of oxidative stress. The results of this study indicate that kidney is more vulnerable to the caused by vanadium and/or nickel-induced oxidative stress than liver, the oxidative capacity of nickel is much lower than vanadium as well as that the oxidative capacity of combined vanadium and nickel may be more markedly decreased than at separate exposure.
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