Kurtoglu, Firuze;Kurtoglu, Varol;Sivrikaya, Abdullah
Asian-Australasian Journal of Animal Sciences
/
v.21
no.6
/
pp.883-889
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2008
Lipid peroxidation (LPO) has been identified as an important component of atherosclerosis. In this study, the effects of supplementation with cholesterol (0.5%), olive oil (5%) and vitamin E (0.05%) on erythrocyte glutathione (GSH), plasma malondialdehyde (MDA), total cholesterol, HDL-LDL cholesterol and triacylglycerol, brain and liver MDA and GSH concentrations of rats were investigated. A total of 50 Sprague-Dawley male rats aged 6 months, and of equal body weight were used and fed a standard ration ad libitum. Animals were housed in the University of Selcuk, Veterinary Faculty Experimental Animals Unit. The experiment lasted 60 days and there were five experimental groups as follows: 1. Control, 2. Cholesterol (0.5%), 3. Olive oil (5%), 4. Cholesterol plus vitamin E (0.05%), 5. Olive oil plus vitamin E (0.05%). At the end of the experiment, blood samples were taken by cardiac puncture and erythrocyte GSH, plasma MDA, cholesterol, HDL-LDL cholesterol, triacylglycerol and also GSH and MDA concentrations in brain and liver tissue of rats were spectrophotometrically determined. Supplementation of olive oil and cholesterol into rat diets (groups 2 and 3) caused significant differences in lipid parameters; HDL cholesterol concentrations were increased in the olive oil group and LDL cholesterol was lower than in the cholesterol fed group. Moreover, these decreases in LDL and triacylglycerol concentrations were more significant with vitamin E supplementation. The high plasma MDA concentrations showed that lipid peroxidation occurred in the olive oil group and the highest brain MDA concentrations were determined also in the olive oil group. These findings suggest that vitamin E addition may decrease the sensitivities of several oils to oxidation and that monounsaturated fatty acids in olive oil may decrease the incidence of atherosclerosis by regulating blood lipid profiles.
Bayril, T.;Yildiz, A.S.;Akdemir, F.;Yalcin, C.;Kose, M.;Yilmaz, O.
Asian-Australasian Journal of Animal Sciences
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v.28
no.8
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pp.1133-1139
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2015
This study aimed to determine the effects of parenteral selenium (Se) and vitamin E supplementation on economic impact, milk yield, and some reproductive parameters in high-yield dairy cows in the dry period and in those at the beginning of lactation. At the beginning of the dry period, cows (n = 323) were randomly divided into three groups as follows: Treatment 1 (T1), Treatment 2 (T2), and Control (C). Cows in group T1 received this preparation 21 days before calving and on calving day, and cows in group T2 received it only on calving day. The cows in the control group did not receive this preparation. Supplementation with Se increased Se serum levels of cows treated at calving day (p<0.05). Differences in milk yield at all weeks and the electrical conductivity values at the 8th and 12th weeks were significant (p<0.05). Supplementation with Se and Vitamin E decreased the incidence of metritis, the number of services per conception and the service period, but had no effects on the incidence of retained fetal membrane. A partial budgeting analysis indicated that Se supplementation was economically profitable; cows in group T1 averaged 240.6$ per cow, those in group T2 averaged 224.6$ per cow. Supplementation with Se and Vitamin E has been found to increase serum Se levels, milk yield, and has positive effects on udder health by decreasing milk conductivity values and incidence of sub-clinical mastitis.
We investigated the effects of vitamin E supplementation on protein glycosylation in early and end stage product, and light microscopic studies were done on the renal glomeruli of KK-mice of various ages and various duration of diabetes. Weaned KK-mice were fed high fat diets containing 20% corn oil(wt/wt), and sacrificed at 4,6, and 9 months of age. The high vitamin E diet was a high fit diet supplemented with an excess amount of d1-$\alpha$-tocopheryl acetate (2080IU/kg diet). We measured Hemoglobin $A_{IC}$ (Hb $A_{IC}$) as a glycosylation early product, and renal collagen-linked fluorescence as a glycosylation end product. In the diabetic group, levels of Hb $A_{IC}$ were increased within 2 months after onset of diabetes and remained at a constant level for the duration of experiment. 5 months after onset of diabetes, renal collagen linked fluorescence(CLF) was markedly increased. A quantative, morphologically demonstratable, progressive thickening of the basement membrane and calcification occured in the diabetic KK-mice. There is a statiscally positive correlation between CLF and histologic grade of diabetic nephropathy. Hepatic vitamin E levels correlated with those of Hb $A_{IC}$, renal CLF, and renal calcification. Treatment with vitamin I did not modify the level of blood glucose. However, we observered a significant lowering of CLF and Hb $A_{IC}$ in diabetic mice. Supplementation of vitamin E was found to delay the progression of diabetic nephropathy. (forean J Nutrition 31(6) : 1024-1030, 1998)0, 1998)
The purpose of this study was to investigate the effect of vitamin E and selenium on the antioxidative defense mechanism in the liver of streptozotocin(STZ)-induced diabetic rats. Sprague-Dawley male rats(120$\pm$10gm) were randomly assigned to one control and five STZ-diabetic groups. Diabetic groups were classified to STZ-0E (vitamin E free diet), STZ-40E(40mg vitamin E/kg of diet), STZ-400E(400mg vitamin E/kg of diet), STZ-S(0.5ppm Se/kg of diet) and STZ-400ES(400mg vitamin E and 0.5ppm Se/kg of diet) according to the level of vitamin E and selenium supplementation. Diabetes was experimentally induced by intravenous adminstration of 55mg/kg of STZ in citrate buffer(pH 4.3) after 4-weeks feedng of six experimental diets. Animals were sacrificed at the 4th day of diabetic states. Activities of the serum glutamic oxaloacetate transaminase(GOT) and the glutaminc pyruvate transaminase(GPT) in STZ-0E, STZ-40E and STZ-S rats were higher than those of control. Liver xanthine oxidase activities were similar to serum GOT and GPT. Liver superoxide dismutase(SOD) activities were higher in STZ-0E and STZ-40E groups by 33%, 22%, respectively than that of control. Glutathione S-transferase(GST) activities of liver were similar to GSH-Px activities. The contents of vitamin E in liver tissue were significantly lower STZ-0E, STZ-40E and STZ-S groups by 50%, 36%, 45% than that of control. Reduced glutathione(GSH) contents of liver were lower STZ-0E, STZ-40E, STZ-400E, STZ-S and STZ-400ES groups by 57%, 51%, 19%, 18%, 12% than that of control. Lipid peroxide values (LPO) in liver were higher 5.6, 2.3 and 2.3 times in STZ-0E, STZ-40E and STZ-S group than that of control. The present results indicate that STZ-induced diabetic rats are more sensitive to oxidative stress, leading to the acceleration of lipid peroxidation process, which can be more accelerated by feeding the low level of dietary vitamin E. In the coincident supplementation of high dietary vitamin E and selenium antioxidative enzymes activities and physiolosical antioxidants were increased more than those of the separate supplementation of vitamin E or selenium. Therefore, dietary vitamin E and selenium reduced peroxidative damage of tissue, promoting antioxidative defense mechanism against lipid peroxidation by diabetes.
1. For the prophylaxis of ceroidosis Vitamin E and C supplemented diet(POV 90.4mEg/kg) was used for flounder culture during 80 days. 2. The supplementation of Vitamin E and C with our tested concentrations on the high POV diet supported almost normal growth of flounder. It is very much comparable with the abnormal growth of flounder fed the diet of high POV. 3. The best prophylactic effect were appeared the high POV diet supplemented with Vitamin E 1mg/g diet and Vitamin C 2IU/g diet. These results were analyzed by histological observation of tissues.
We compared the preventive capacity of high intakes of vitamin C (VC) and vitamin E (VE) on oxidative stress and liver toxicity in rats fed a low-fat ethanol diet. Thirty-two Wistar rats received the low fat (10% of total calories) Lieber-DeCarli liquid diet as follows: either ethanol alone (Alc group, 36% of total calories) or ethanol in combination with VC (Alc + VC group, 40 mg VC/100 g body weight) or VE (Alc + VE group, 0.8 mg VE/100 g body weight). Control rats were pair-fed a liquid diet with the Alc group. Ethanol administration induced a modest increase in alanine aminotransferase (ALT), aspartate aminotransferase (AST), conjugated dienes (CD), and triglycerides but decreased total radical-trapping antioxidant potential (TRAP) in plasma. VE supplementation to alcohol-fed rats restored the plasma levels of AST, CD, and TRAP to control levels. However, VC supplementation did not significantly influence plasma ALT, AST, or CD. In addition, a significant increase in plasma aminothiols such as homocysteine and cysteine was observed in the Alc group, but cysteinylglycine and glutathione (GSH) did not change by ethanol feeding. Supplementing alcohol-fed rats with VC increased plasma GSH and hepatic S-adenosylmethionine, but plasma levels of aminothiols, except GSH, were not influenced by either VC or VE supplementation in ethanol-fed rats. These results indicate that a low-fat ethanol diet induces oxidative stress and consequent liver toxicity similar to a high-fat ethanol diet and that VE supplementation has a protective effect on ethanol-induced oxidative stress and liver toxicity.
Objective: Adequate vitamin and trace mineral intake for pigs are important to achieve satisfactory growth performance. There are no data available on the vitamin and trace mineral intake across pig producers in China. The purpose of this study was to investigate and describe the amount of vitamin and trace minerals used in Chinese pig diets. Methods: A 1-year survey of supplemented vitamin and trace minerals in pig diets was organized in China. A total of 69 producers were invited for the survey, which represents approximately 90% of the pig herd in China. Data were compiled by bodyweight stages to determine descriptive statistics. Nutrients were evaluated for vitamin A, vitamin D, vitamin E, vitamin K, thiamine, riboflavin, vitamin B6, vitamin B12, pantothenic acid, niacin, folic acid, biotin, choline, copper, iron, manganese, zinc, selenium, and iodine. Data were statistically analyzed by functions in Excel. Results: The results indicated variation for supplemented vitamin (vitamin A, vitamin D, vitamin E, vitamin K, vitamin B12, pantothenic acid, niacin, and choline) and trace minerals (copper, manganese, zinc, and iodine) in pig diets, but most vitamins and trace minerals were included at concentrations far above the total dietary requirement estimates reported by the National Research Council and the China's Feeding Standard of Swine. Conclusion: The levels of vitamin and trace mineral used in China's pig industry vary widely. Adding a high concentration for vitamin and trace mineral appears to be common practice in pig diets. This investigation provides a reference for supplementation rates of the vitamins and trace minerals in the China's pig industry.
This study was performed to assess the nutritional status of nursing home residents and to assess the effect of nutrition intervention. The subjects were 123 people aged over 60 years from 5 different nursing homes. The nutrition intervention study was carried out by supplementing their diet with multivitamin-minerals for 2 months. The mean intakes of most nutrients did not meet the RDA, Though the nutrient content of the menus provided by the facilities were satisfactory. Nutrients of which intakes fell below 75% of the RDA were protein, Ca, Fe, vitamin A vitamin B$_1$, and vitamin B$_2$. The BMIs of male and female subjects were 22.0kg/$m^2$ and 24.6kg/$m^2$ and the WHRs were 0.92 and 0.90, respectively. The percentage of subjects with hypertention (BP$\geq$140/90mmHg) and with anemia(Hb$\leq$13mg/100$m\ell$ in men, Hb$\leq$12mg/100$m\ell$ in women) were 34.6% and 41.9%, respectively. The serum cncentrations of albumin, total protein, triglyceride, total cholesterol, HDL-cholesterol, and total lipid fell within normal ranges. However, 27.5% of the subjects showed a high serum cholesterol level of over 250mg/100$m\ell$. The concentration of C3 was 81.2mg/100$m\ell$, IgG, 1343mg/100$m\ell$, and IL-2, 0.766mg/$m\ell$. after 2 months of vitamin-mineral supplementation, the levels of blood glucose and total cholesterol were significantly decreased and triglyceride was significantly increased. The vitamin-mineral supplementation had no effect on the mean levels of vitamin A and E, IgG, IL2, and C3. However, the intervention resulted int he improvement of serum vitamin A and E levels when the subject\`s serum levels were low before the supplementation.
The present study was designed to determine long-term feeding effects of vitamin E and BHT (butylated hydroxytoluene) on serum biochemical profiles, organ weight, and intestinal and hepatic antioxidant enzymes including superoxide dismutase (SOD), glutathione peroxidase (GSH-PX), and glutathione-S-transferase (GST) in ICR mice. Four wk old ICR mice (n=8 per group) were fed the diets supplemented with vitamin E (I ; 0.03% and II ; 0.3%) and BHT (I ; 0.05% and II ; 0.5%) for 12 months. Feeding the diets containing vitamin E and BHT had no effects on growth and serum biochemical profiles. However, feeding the diets supplemented with 0.5% BHT for 12 months significantly increased liver weight of the mice. In the small intestine, there were no effects of vitamin E or BHT on SOD and GSH-PX activities in the mucosa. However, the activity of intestinal GST of the mice that received 0.5% BHT was almost twice as high as that of control mice. In the liver, the activity of SOD was not affected by feeding antioxidants for 12 months, whereas GSH-PX activity was significantly increased in mice that received the diets containing BHT (0.05%, 0.5%) and vitamin E (0.03%, 0.3%). In addition, supplementation of 0.5% BHT markedly enhanced hepatic GST activity compared with other groups. Enhanced activity of GSH-PX in response to feeding vitamin E or BHT might aid hepatic enzymes to eliminate active oxygen in organs from mice. However, we could not exclude the possibility of increased lipid peroxidation by high dosage of BHT supplementation. More detailed study is necessary for assessment of preventive or toxicological effects of high dosage of BHT supplementation.
The present study was conducted to evaluate effects of the increased dietary vitamin A supplementation on the vitamin A, vitamin E and ascorbic acid concentrations in the plasma and liver and activities of some enzymes in the liver of the growing chicken. One hundred and twenty female chickens at 4 weeks of age were divided in 6 equal groups in accordance with their body weight. They were housed in cages and fed on standard wheat-barley-based broiler diet balanced in the major nutrients. Vitamin A was supplemented in the form of retinyl acetate. Control diet was supplemented with 10 IU/g and experimental feeds were supplemented with 50, 100, 500, 1000 and 2000 IU/g. At days 42 and 56 of the development 8 chickens from each group were killed, plasma and liver were collected for vitamin and enzyme analyses. The increased vitamin A supplementation was associated with its increased accumulation in the liver and with a reduction of ${\alpha}-tocopherol$ concentrations in the plasma and liver. The blood plasma was more resistant to vitamin A concentration changes and the retinol level was elevated only when the vitamin A dose exceeded 100 IU/g feed. Ascorbic acid concentration in the liver was elevated when moderately high vitamin A supplementation was used but significantly decreased at the highest vitamin A dose. Similar changes were observed with glycogen concentration in the liver. Activities of hexokinase, glucose-6-phosphatase and lactate dehydrogenase in the chicken liver were also dependent on vitamin A supplementation, decreasing with highest vitamin A doses. Therefore the observations showed that the vitamin A excess compromises antioxidant system of the growing chickens suggesting that prooxidant activity may be responsible for at least part of the toxicity of vitamin A.
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