In this study, the effect of vitamin E plus selenium (Se) application on malondialdehyde (MDA), glutathione (GSH), vitamin E, C, A and -carotene were aimed to investigate in exercised horses. For this purpose, 50 healthy Anatolian type local horse breed aged between 3-5 from Altındere Study Farm were used. The animals were divided into two equal groups. While 1st group received nothing, horses in second group were received vitamin E+Se intramuscularly. Then animals in both groups were exercised for 1500 meters. Blood samples were taken handily from all animals before and after exercise. This samples were analyzed for MDA, GSH, vitamin E, C, A and β-caroten spectrophotometrically.MDA and GSH concentration in 1st group were found to increase significantly (p<0.001) after exercise. On the other hand, serum vitamin E, C, A and β-carotene levels did not changed significantly. In the second group, serum vitamin E levels increased significantly (p<0.001) after vitamin E+selenium application. Furthermore, MDA (p<0.05) and GSH (p<0.001) levels increased significantly after exercise in the second group. Vitamin E levels decreased significantly (p<0.01) after exercise. However, vitamin A and C levels did not change significantly. In addition, in the second group, β-carotene levels were also changed significantly (p<0.05) when the values obtained before vitamin E application compared with the values obtained after vitamin E application. When comparison made between groups, while MDA and vitamin E values were statistically important (p<0.05), GSH, vitamin C, A and β-carotene values were not important statisticallyAs a result, acute exercise can increase free-radical production which, the results shows that increase in both MDA and GSH can be shown as the indicator of it. Furthermore, decrease in MDA level in vitamin E applied group the indicator of the rise in antioxidant defense and protective effect of vitamin E.

Stress is commonly used to describe the detrimental effectsof a variety of conditions surrounding animals on their health performance. Environmental stress causes an increasein oxidative stress and an imbalance in antioxidant status. Oxidative damage increases in stressed poultry when the plasma antioxidant vitamins and minerals such as vitamin C, E, folic acid, and zinclevels declined. Stress factors in birds involve many elements of the transport processes which may be detrimental to the birds. These factors include alteration in atmospheric temperature, poor handlingby man, removal of feed and water (starvation), high ambient temperature (AT) and relative humidity (RH). Other factors incude vaccination, disease conditions such as coccidiosis, novelty,confinement, motion, noise, microthermal core within the vehicle and the use of inappropriate vehicles. Live birds of all ages are being transported mainly by roads to their various destinations and across different ecological zones throughout the year. Mortality increaseswith journey length. The adverse effects of these factors and their combinations may range from mild discomfort and aversion to death. This review was aimed at providing comprehensive information on the role of vitamin C in combating stress factors in poultry with the view of exploring its potentials for future research undertaking.Information compiled in this review were obtained from search engines such as Elsevier, Pubmed, Springer, Medline, Science Direct, Google Scholar, and a library search for articles published in peerreviewedjournals. 100 to 200 mg/kg feed of vitamin C is capable of converting stress factors in poultry and thereby improving the productivity.

Mannheimia haemolytica is an important cause of pneumonia in feedlot cattle. Nuclear factor erythroid-2-related factor 2 (Nrf2) is a redox-sensitive transcription factor responsible for the induction of antioxidant enzymes, such as heme oxygenase 1 (HO-1), within the lung. The expression of Nrf2 and HO-1 was immunohistochemically evaluated in 4 calves 24 h after experimental infection with M. haemolytica. Calves receiving normal saline served as controls. In the infected lungs, cytoplasmic Nrf2 expression was high in macrophages and bronchioles and low in alveolar epithelium, whereas nuclear expression was high in endothelial cells, macrophages, and bronchioles and lowest in alveolar epithelium. Normal lung samples displayed only faint Nrf2 cytoplasmic staining within bronchiolar epithelium. Expression of HO-1 was detected within the cytoplasm of macrophages and bronchiolar epithelial cells in all infected lung samples, whereas normal lungs displayed only weak cytoplasmic staining in bronchiolar epithelial cells. These findings suggest that bronchiolar epithelial cells and macrophages up-regulate Nrf2 expression early in the course of infection, which results in increased expression of HO-1 within these cells.

To assess right colic artery blood flow and relevance of xanthine dehydrogenase/xanthine oxidase after experimentally induced strangulation obstruction and reperfusion of the colon, 5 ponies were subjected to 2.5 hours of complete ischemia of the left dorsal and ventral colons, allowed to recover from surgery, and monitored during a 48-hour reperfusion period. Five ponies were subjected to sham surgery and served as controls. All ponies had a Doppler ultrasound blood flow monitor implanted on the right colic artery near the pelvic flexure 10 to 14 days prior to the ischemic period. Colic artery blood flow was monitored prior to, during, and for 4 hours after surgery. Blood samples from the right colic artery and vein distal to the obstruction site were collected during surgery (prior to ischemia, after 1 and 2 hours of ischemia, and after 10 and 60 minutes of reperfusion) for determination of arterial and venous blood gas tensions and electrolytes. Prior to surgery, blood selenium and plasma vitamin E (alpha-tocopherol) concentrations and blood glutathione peroxidase (GPX) activity were determined to assess the status of endogenous antioxidants. Combined xanthine dehydrogenase (XDH) plus xanthine oxidase (XO) activity, and XO activity alone (nanomoles per minute per gram of tissue) were determined, using a dual-spectrophotometric technique. Xanthine dehydrogenase and oxidase activities were determined prior to ischemia, after 1 and 2 hours of ischemia, and at 1 and 48 hours after reperfusion. Median blood flow in the experimental and control groups (156 ml/min and 110 ml/min, respectively) was not statistically different before surgery, and was significantly (P < 0.02) lower in the experimental (4 ml/min) vs the control group (72.5 ml/min) during the ischemic period. Experimental ponies had significantly (P < 0.03) lower right colic artery blood flow during the 4 hours immediately after recovery from anesthesia. Significant difference was not observed in right colonic venous bicarbonate concentration between groups at any time. Median right colonic venous P(CO2), pH, and standard base excess were different (P < 0.001) between groups during the ischemic period only. Median venous oxygen saturation and median venous P(O2) were significantly (P < 0.001) lower in the experimental ponies at the end of 2 hours of ischemia, but were significantly (P < 0.05) increased during the reperfusion phase. Median venous potassium concentration was significantly (P < 0.01) higher in experimental ponies during the ischemic and reperfusion phases. Vitamin E and GPX values were within normal limits for all ponies. Median selenium concentration was < 15 microgram/dl; however, there were no significant differences between control and experimental ponies. Only 3 of 10 ponies had measurable XHH/XO activity at the beginning of the experiment. Enzyme activity was detected in 1 additional pony during the ischemic period. However, in all 4 ponies in which XDH/XO activity was detected, enzyme activity was low (10 to 36 nmol/min/g). On the basis of macroscopic and histologic examination of the large colon, evidence of reperfusion injury was not found in 4 of the 5 experimental ponies. The only pony with gross evidence of reperfusion injury did not have detectable XO activity. Results of the study indicate that hypoperfusion of the colon during the postischemic period may be a factor in deterioration of the colon observed clinically in equids with surgical correction of large-colon volvulus. Additionally, if reperfusion injury develops in the large colon, it probably is not mediated through the xanthine oxidase enzyme system: the activity of this enzyme in the large colon, when present, is negligible.

Monensin is an ionophoretic antibiotic, which selectively transports alkali metal cations across biological membranes. In growing swine, monensin toxicosis causes acute, degenerative cardiac and skeletal myopathy resembling vitamin E-selenium deficiency. Selenium is an essential trace element incorporated in glutathione peroxidase (GSH-Px), an antioxidant enzyme system that protects subcellular membranes. In our study, we examined the effects of monensin on body weight, Se balance, antioxidant status, and serum concentrations of selected minerals in growing pigs that were genetically hypo- or hyperselenemic (hypo-Se and hyper-Se, respectively). Three groups of eight 8-week-old pigs, each comprised of 4 hypo-Se and 4 hyper-Se pigs (76.4 +/- 3.0 and 106.3 +/- 10.3 ng of Se/ml of serum, respectively), were fed standard diets containing 0.1 mg of supplemental Se/kg of body weight, and either 0, 200, or 400 mg of monensin/kg for a 77-day period, followed by a 28-day monensin withdrawal period. On days 0, 7, 28, 56, 70, and 98, all pigs were weighed and blood was collected for determination of serum GSH-Px, creatine phosphokinase, and aspartate transaminase values, as well as serum concentrations of vitamin E, Se, Ca, Cu, Fe, K, Mg, Na, P, and Zn. Significance of main effects of monensin treatment, genetic Se status, and their interactions was tested by Fisher's variance ratio test, followed by conditional comparison of treatment means with a Bonferroni test. Signs of monensin toxicosis were not observed and monensin consumption had no effect on body weight, or serum creatine phosphokinase, aspartate transaminase, or Se values. However, pigs consuming monensin had consistently higher serum GSH-Px activities, possibly because of increased synthesis of this adaptive antioxidant enzyme. Interactions were not found between monensin and genetic Se status. Hyperselenemic pigs were heavier and had higher serum Se and GSH-Px values than hypo-Se pigs. Furthermore, hypo-Se and hyper-Se pigs were hypo- and hypercupremic, respectively, suggesting genetic regulation of copper status. It is likely that pigs with inadequate antioxidant status (hyposelenemia, hypocupremia) are more susceptible to diseases associated with cellular membrane damage, such as vitamin E-Se deficiency disease and monensin toxicosis.

The scavenging of superoxide radicals by endogenous and therapeutically administered superoxide dismutases may prevent superoxide-mediated oxidative stress leading to lipid peroxidation, membrane lysis, and cell death in a wide variety of normal and pathologic states. Simple inorganic manganous salts such as MnCl2 also have superoxide dismutase-like activity and are extremely inexpensive, compared with enzymatic superoxide dismutase preparations. In this study, we explored the use of Mn salts as antioxidant drugs. We used the percentage of inhibition of nitroblue tetrazolium reduction by superoxide as a measure of the amount of superoxide dismutase-like activity. We found concentration-related increases in superoxide scavenging activity in simple buffer solutions upon addition of 1.25, 2.5, and 5.0 microM MnSO4. To determine whether Mn salts can inhibit oxidative damage in tissues, we used an in vitro model of lipid peroxidation in ischemic and reoxygenated rat liver slices. Concentrations of 10, 100, and 1000 micromoles MnCl2/L of buffer significantly decreased indicators of lipid peroxidation believed to be initiated by intracellular superoxide. We then determined the effectiveness of MnCl2 as a superoxide scavenger in conscious horses by measuring the superoxide scavenging ability of equine plasma before and during intravenous infusions of 1.0 L volumes of 0.9% saline solution containing 0, 12.5, or 25 mM MnCl2. Plasma Mn concentrations, which were determined by atomic absorption spectrophotometry, increased as a function of time and dose. Intravenously administered MnCl2 concomitantly produced dose-related increases in superoxide scavenging ability of equine plasma at 15, 30, 45, and 60 minutes after the onset of infusion, compared with preinfusion control values. Heart rate and blood pressure of the treated horses, which were monitored to measure toxicity of MnCl2, gradually increased in both treatment groups. Clinical adverse effects of MnCl2 administration included defecation, pawing, hyperexcitability, flank watching, and sweating. The results of this study indicate that simple Mn salts may scavenge superoxide radicals in vivo with minimal adverse reactions and at a trivial cost.

Therapeutic and anti-oxidant potential of vitamin E and selenium was evaluated in mastitic cows. The CMT point score and milk somatic cell count (SCC) was significantly (P0.05) higher in mastitic cows prior to treatment. Reduced activity of enzymatic anti-oxidant catalase was observed in mastitic animals. The parameters studied in mastitic cows treated amoxicillin sulbactum (group II) and with amoxicillin sulbactum, vitamin E and selenium (group III) were compared with that of group I healthy cows. Significant reduction (P0.05) in CMT and SCC was observed in both the treated groups. However, reduction in CMT point score and SCC was more pronounced in group III than group II cows. Synergistic action of antibiotic and vitamin E selenium significantly (P0.05) enhanced the activity of catalase in group III mastitic animals on day 8 time period. Therefore, vitamin E and selenium supplementation could be advised in the therapy of mastitis.

This article summarizes the different types of free radicals, antioxidants and the effect of oxidative stress on the activities of glutathione peroxidase and glucose 6-phosphate dehydrogenase in bovine liver diseases. A growing body of evidence suggests that the formation of reactive oxygen species is a common occurrence associated with most if not all disease processes. The overall importance of reactive oxygen species to the progression and severity of various disease states varies greatly depending on the conditions and whether the disease is acute or chronic. Free radical researches in animals are in progress and further investigations are needed to establish the involvement of reactive oxygen species in diseases affecting different animal species and the pathology they produce.

Oxidative stress is a common mechanism contributing to initiation and progression of hepatic damage in a variety of liver disorders. Hence, there is a great demand for the development of agents with potent antioxidant effect. The aim of the present investigation is to evaluate the efficacy of raw and nanoforms of resveratrol and silibinin as a hepatoprotective and an antioxidant against diethylnitrosamine induced hepatocellular damage. 0.01% diethylnitrosamine administration to rats resulted in significantly elevated levels of lipid peroxidation (LPO) and decreased levels of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX), glutathione reductase (GSH) and total protein (TP) in the liver tissue. Post-treatment with the nano resveratrol (50 mg/kg), nano silibinin (50 mg/kg), raw resveratrol (50 mg/kg), raw silibinin (50 mg/kg) orally for 30 days significantly reversed the diethylnitrosamine induced alterations in the liver tissue and offered almost complete protection. The results from the present study indicate that both nano forms exhibit good hepatoprotective and antioxidant potential against diethylnitrosamine induced hepatocellular damage in rats as compared to raw forms.