scholarly journals Reduction of Dexamethasone-Induced Oxidative Stress and Lipid Peroxidation in Laying Hens by Dietary Vitamin E Supplementation

2008 ◽  
Vol 20 (2) ◽  
pp. 28 ◽  
Author(s):  
Y Eid ◽  
T Ebeid ◽  
M Moawad ◽  
M ElHabbak
1995 ◽  
Author(s):  
Joseph Kanner ◽  
Dennis Miller ◽  
Ido Bartov ◽  
John Kinsella ◽  
Stella Harel

Biological oxidations are almost exclusively metal ion-promoted reactions and in ths respect iron, being the most abundant, is the commonly involved. The effect of dietary iron levels on pork, turkey and chick muscle lipid peroxidation and various other related compounds were evaluated. Crossbred feeder pigs were fed to market weight on corn-soy rations containing either 62, 131 or 209 ppm iron. After slaughter, the muscles were dissected, cooked and stored at 4°C. Heavily fortifying swine rations with iron (>200 ppm) increase nn-heme iron (NHI), thiobarbituric acid reactive substances (TBARS), and decrease a-tocopherol in cooked stored pork but did not increase warmed-over aroma (WOA). NHI and TBARS were higher in cooked pork from pigs fed high-iron diets. Liver iron correlated with muscle iron. TBARS were strongly related with WOA. The role of dietary vitamin E and ascorbic acid on Fe-induced in vivo lipid peroxidation in swine was also evaluated. Moderate elevation in iron stores had a marked effect on oxidative stress, especially as indicated by liver TBARS. Supplemental vitamin E, and to a lesser extent vitamin C, protect against this oxidative stress. Unsupplementation of Fe in the regular diet of turkeys did not affect body weight, blood hemoglobin level, or iron pool in the liver or muscle. The reason being that it contained "natural" ~120 mg Fe/kg feed, and this amount is high enough to keep constant the pool of iron in the body, liver or muscle tissues. Only Fe-supplementation with high amounts of Fe (500 ppm) significantly increased turkey blood hemoglobin and total iron in the liver, in 1 out of 3 experiments, but only slightly affects iron pool in the muscles. It seems that the liver accumulates very high concentations of iron and significantly regulates iron concentration in skeletal muscles. For this reason, it was very difficult to decrease muscle stability in turkeys through a diet containing high levels of Fe-supplementation. It was shown that the significant increase in the amount of iron (total and "free") in the muscle by injections with Fe-dextran accelerated its lipid peroxidation rate and decreased its a-tocopherol concentration. The level and metabolism of iron in the muscles affects the intensity of in vivo lipid peroxidation. This process was found to ifluence the turnover and accumulation of a-tocopherol in turkey and chick muscles. Treatments which could significantly decrease the amount and metabolism of iron pool in muscle tissues (or other organs) may affect the rate of lipid peroxidation and the turnover of a-tocopherol. Several defense enzymes were determined and found in the turkey muscle, such as superoxide dismutase, catalase, and glutathione peroxidase. Glutathione peroxidase was more active in muscles with a high trend of lipid peroxidation, lmore so in drumsticks than in breast muscles, or muscles with a low a-tocopherol content. The activity of glutathione peroxidase increased several fold in muscle stored at 4°C. Our work demonstrated that it will be much more practical to increase the stability of muscle tissues in swine, turkeys and chickens during storage and processing by increasing the amount of vitamin E in the diet than by withdrawing iron supplementation.


2000 ◽  
Vol 11 (3) ◽  
pp. 539-549
Author(s):  
JOHANNES M. ROOB ◽  
GHOLAMALI KHOSCHSORUR ◽  
ANDREAS TIRAN ◽  
JÖRG H. HORINA ◽  
HERWIG HOLZER ◽  
...  

Abstract. Intravenous iron application to anemic patients on hemodialysis leads to an “oversaturation” of transferrin. As a result, non-transferrin-bound, redox-active iron might induce lipid peroxidation. To test the hypothesis that vitamin E attenuates lipid peroxidation in patients receiving 100 mg of iron(II) hydroxide sucrose complex intravenously during a hemodialysis session, 22 patients were investigated in a randomized cross-over design, either with or without a single oral dose of 1200 IU of all-rac-α-tocopheryl acetate taken 6 h before the hemodialysis session. Blood was drawn before and 30, 60, 90, 135, and 180 min after the start of the iron infusion, and areas under the curve (AUC0-180 min) of ratios of plasma malondialdehyde (MDA) to cholesterol and plasma total peroxides to cholesterol (two markers of lipid peroxidation) were determined as the outcome variables. At baseline of the session without vitamin E supplementation, plasma α-tocopherol concentrations (27.6 ± 1.8 μmol/L) and ratios of α-tocopherol to cholesterol (5.88 ± 1.09 mmol/mol) were normal, plasma MDA concentrations were above normal (1.20 ± 0.28 μmol/L), and bleomycin-detectable iron (BDI), indicating the presence of redox-active iron, was not detectable. Upon iron infusion, BDI and MDA concentrations increased significantly (P < 0.001). BDI concentrations explained the increase over baseline in MDA concentrations (MDA = 1.29 + 0.075 × BDI). Vitamin E supplementation, leading to a 68% increase in plasma α-tocopherol concentrations, significantly reduced the AUC0-180 min of MDA to cholesterol (P = 0.004) and peroxides to cholesterol (P = 0.002). These data demonstrate that a single oral dose of vitamin E attenuates lipid peroxidation in patients on hemodialysis receiving intravenous iron. Given that intravenous iron is applied repeatedly to patients on hemodialysis, this therapeutic approach may protect against oxidative stress-related degenerative disease in the long term.


1997 ◽  
Vol 83 (1) ◽  
pp. 189-195 ◽  
Author(s):  
Chandan K. Sen ◽  
Mustafa Atalay ◽  
Jyrki Ågren ◽  
David E. Laaksonen ◽  
Sashwati Roy ◽  
...  

Sen, Chandan K., Mustafa Atalay, Jyrki Ågren, David E. Laaksonen, Sashwati Roy, and Osmo Hänninen. Fish oil and vitamin E supplementation in oxidative stress at rest and after physical exercise. J. Appl. Physiol.83(1): 189–195, 1997.—Fish oil supplementation and physical exercise may induce oxidative stress. We tested the effects of 8 wk of α-tocopherol (vitamin E) and fish oil (FO) supplementation on resting and exercise-induced oxidative stress. Rats ( n = 80) were divided into groups supplemented with FO, FO and vitamin E (FOVE), soy oil (SO), and SO and vitamin E (SOVE), and for FOVE and SOVE they were divided into corresponding exercise groups (FOVE-Ex and SOVE-Ex). Lipid peroxidation [thiobarbituric acid-reacting substances (TBARS)] was 33% higher in FO compared with SO in the liver, but oxidative protein damage (carbonyl levels) remained similar in both liver and red gastrocnemius muscle (RG). Vitamin E supplementation, compared with FO and SO, markedly decreased liver and RG TBARS, but liver TBARS remained 32% higher in FOVE vs. SOVE. Vitamin E also markedly decreased liver and RG protein carbonyl levels, although levels in FOVE and SOVE were similar. Exercise increased liver and RG TBARS and RG protein carbonyl levels markedly, with similar levels in FOVE-Ex and SOVE-Ex. FO increased lipid peroxidation but not protein oxidation in a tissue-specific manner. Vitamin E markedly decreased lipid peroxidation and protein oxidation in both FOVE and SOVE, although liver lipid peroxidation remained higher in FOVE. Despite higher levels of hepatic lipid peroxidation at rest in FOVE compared with SOVE, liver appeared to be relatively less susceptible to exercise-induced oxidative stress in FOVE.


2001 ◽  
Vol 46 (No. 5) ◽  
pp. 140-144 ◽  
Author(s):  
K. Sahin ◽  
N. Sahin ◽  
M. Onderci ◽  
S. Yaralioglu ◽  
O. Kucuk

An experiment utilizing Cobb-500 male broilers was conducted to evaluate the effects of vitamin E supplementation at various concentrations on malonyldialdehyde (MDA) as an indicator of lipid peroxidation, serum and liver concentrations of antioxidant vitamins and some minerals of broilers reared under heat stress (32&deg;C). One day-old 150 male broilers were randomly assigned to 5 treatment groups, 3 replicates of 10 birds each. The birds received either a basal diet or basal diet supplemented with vitamin E (dl-a-tocopherol acetate) at 62.5, 125, 250, or 500 mg/kg of diet. Increased supplemental vitamin E linearly increased serum vitamin E and A, but decreased (P&nbsp;= 0.001) MDA concentrations. Increasing dietary vitamin E supplementation also resulted in linear increases in liver vitamin E and A concentrations, but linear decreases in MDA concentrations (P&nbsp;= 0.01). Increasing dietary vitamin E caused a linear increase in serum concentrations of Fe and Zn (P= 0.001), but a decrease in serum concentration of Cu (P&nbsp;= 0.001). Results of the present study conclude that in broiler chicks reared under heat stress a 250 mg of vitamin E supplementation can be considered as a protective management practice in a broiler diet, reducing the negative effects of heat stress.


2002 ◽  
Vol 3 (3) ◽  
pp. 185-192 ◽  
Author(s):  
Randall L. Davis ◽  
Christy L. Lavine ◽  
Melissa A. Arredondo ◽  
Patrick McMahon ◽  
Thomas E. Tenner, Jr.

Determination of reliable bioindicators of diabetes-induced oxidative stress and the role of dietary vitamin E supplementation were investigated. Blood (plasma) chemistries, lipid peroxidation (LPO), and antioxidant enzyme activities were measured over 12 weeks in New Zealand White rabbits (control, diabetic, and diabetic + vitamin E). Cholesterol and triglyceride levels did not correlate with diabetic state. PlasmaLPOwas influenced by diabetes and positively correlated with glucose concentration only, not cholesterol or triglycerides. Liver glutathione peroxidase (GPX) activity negatively correlated with glucose and triglyceride levels. Plasma and erythrocyte GPX activities positively correlated with glucose, cholesterol, and triglyceride concentrations. Liver superoxide dismutase activity positively correlated with glucose and cholesterol concentration. Vitamin E reduced plasma LPO, but did not affect the diabetic state. Thus, plasmaLPOwas the most reliable indicator of diabetes-induced oxidative stress. Antioxidant enzyme activities and types of reactive oxygen species generated were tissue dependent. Diabetes-induced oxidative stress is diminished by vitamin E supplementation.


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