scholarly journals Evaluation of different vitamin E recommendations and bioactivity of α-tocopherol isomers in broiler nutrition by measuring oxidative stress in vivo and the oxidative stability of meat

2011 ◽  
Vol 90 (7) ◽  
pp. 1478-1488 ◽  
Author(s):  
M. Voljč ◽  
T. Frankič ◽  
A. Levart ◽  
M. Nemec ◽  
J. Salobir
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.


2005 ◽  
Vol 99 (4) ◽  
pp. 1247-1253 ◽  
Author(s):  
José Magalhães ◽  
António Ascensão ◽  
José M. C. Soares ◽  
Rita Ferreira ◽  
Maria J. Neuparth ◽  
...  

Severe high-altitude hypoxia exposure is considered a triggering stimulus for redox disturbances at distinct levels of cellular organization. The effect of an in vivo acute and severe hypobaric hypoxic insult (48 h at a pressure equivalent to 8,500 m) on oxidative damage and respiratory function was analyzed in skeletal muscle mitochondria isolated from vitamin E-supplemented (60 mg/kg ip, 3 times/wk for 3 wk) and nonsupplemented mice. Forty male mice were randomly divided into four groups: control + placebo, hypoxia + placebo (H + P), control + vitamin E, and hypoxia + vitamin E. Significant increases in mitochondrial heat shock protein 60 expression and protein carbonyls group levels and decreases in aconitase activity and sulfhydryl group content were found in the H + P group when compared with the control + placebo group. Mitochondrial respiration was significantly impaired in animals from the H + P group, as demonstrated by decreased state 3 respiratory control ratio and ADP-to-oxygen ratio and by increased state 4 with both complex I- and II-linked substrates. Using malate + pyruvate as substrates, hypoxia decreased the respiratory rate in the presence of carbonyl cyanide m-chlorophenylhydrazone and also stimulated oligomycin-inhibited respiration. However, vitamin E treatment attenuated the effect of hypoxia on the mitochondrial levels of heat shock protein 60 and markers of oxidative stress. Vitamin E was also able to prevent most mitochondrial alterations induced by hypobaric hypoxia. In conclusion, hypobaric hypoxia increases mitochondrial oxidative stress while decreasing mitochondrial capacity for oxidative phosphorylation. Vitamin E was an effective preventive agent, which further supports the oxidative character of mitochondrial dysfunction induced by hypoxia.


2006 ◽  
Vol 52 (2) ◽  
pp. 142-147 ◽  
Author(s):  
Mandava Venkasteswara Rao ◽  
Sheetal Sudhir Parekh ◽  
Sunita Lalchand Chawla

2000 ◽  
Vol 25 (4) ◽  
pp. 274-287 ◽  
Author(s):  
Peter M. Tiidus

Information suggests that there may be gender-based differences in skeletal muscle responses to damaging exercise. Evidence demonstrates that estrogen has strong antioxidant properties and may be an important factor in maintaining postexercise membrane stability and limiting creatine kinase (CK) leakage from damaged muscle in female animals. Research demonstrates effects of estrogen and possible gender differences in other morphological and biochemical indices of postexercise muscle damage and leukocyte invasion. Nevertheless, there are conflicting findings suggesting that in some in vivo exercise models, estrogen administration has limited ability to affect exercise-induced oxidative stress and muscle damage and max cause loss of tissue vitamin C. Gender differences appear to exist in tissue levels of other important antioxidants such as vitamin E and glutathione. More research is needed to fully define the potential for estrogen to influence postexercise muscle damage and the inflammatory response and to determine the mechanisms by which it may operate. Key words: exercise, neutrophils, creatine kinase, vitamin E, vitamin C


1991 ◽  
Vol 65 (04) ◽  
pp. 411-414 ◽  
Author(s):  
Keizo Umegaki ◽  
Hiromi Saegusa ◽  
Masato Kurokawa ◽  
Tomio Ichikawa

SummaryEffects of vitamin E on platelet function and serum lipid peroxide levels were investigated in DOCA-salt hypertensive rats. In the hypertensive rats, ADP- and collagen-induced platelet aggregation in whole blood were markedly attenuated and accompanied by a reduction of serotonin content as compared with the normotensive controls. These facts indicated the appearance of exhausted platelets, which have already been activated in vivo, due to the hypertension. Platelet vitamin E levels were decreased by 50%, while serum lipid peroxide levels were increased 3.6-fold in the hypertensive rats. Vitamin E administration (10 times the dietary intake) during the experimental periods did not influence either the aggregability or the serotonin content of platelets from the hypertensive rats. However, vitamin E administration significantly prevented the elevation of serum tipid peroxides due to the hypertension. These results suggest that vitamin E administration has little effect on platelet activation in vivo due to DOCA-salt hypertension.


2020 ◽  
Vol 31 (1) ◽  
pp. 3-10
Author(s):  
V. S. Nedzvetsky ◽  
V. Ya. Gasso ◽  
A. M. Hahut ◽  
I. A. Hasso

Cadmium is a common transition metal that entails an extremely wide range of toxic effects in humans and animals. The cytotoxicity of cadmium ions and its compounds is due to various genotoxic effects, including both DNA damage and chromosomal aberrations. Some bone diseases, kidney and digestive system diseases are determined as pathologies that are closely associated with cadmium intoxication. In addition, cadmium is included in the list of carcinogens because of its ability to initiate the development of tumors of several forms of cancer under conditions of chronic or acute intoxication. Despite many studies of the effects of cadmium in animal models and cohorts of patients, in which cadmium effects has occurred, its molecular mechanisms of action are not fully understood. The genotoxic effects of cadmium and the induction of programmed cell death have attracted the attention of researchers in the last decade. In recent years, the results obtained for in vivo and in vitro experimental models have shown extremely high cytotoxicity of sublethal concentrations of cadmium and its compounds in various tissues. One of the most studied causes of cadmium cytotoxicity is the development of oxidative stress and associated oxidative damage to macromolecules of lipids, proteins and nucleic acids. Brain cells are most sensitive to oxidative damage and can be a critical target of cadmium cytotoxicity. Thus, oxidative damage caused by cadmium can initiate genotoxicity, programmed cell death and inhibit their viability in the human and animal brains. To test our hypothesis, cadmium cytotoxicity was assessed in vivo in U251 glioma cells through viability determinants and markers of oxidative stress and apoptosis. The result of the cell viability analysis showed the dose-dependent action of cadmium chloride in glioma cells, as well as the generation of oxidative stress (p <0.05). Calculated for 48 hours of exposure, the LD50 was 3.1 μg×ml-1. The rates of apoptotic death of glioma cells also progressively increased depending on the dose of cadmium ions. A high correlation between cadmium concentration and apoptotic response (p <0.01) was found for cells exposed to 3–4 μg×ml-1 cadmium chloride. Moreover, a significant correlation was found between oxidative stress (lipid peroxidation) and induction of apoptosis. The results indicate a strong relationship between the generation of oxidative damage by macromolecules and the initiation of programmed cell death in glial cells under conditions of low doses of cadmium chloride. The presented results show that cadmium ions can induce oxidative damage in brain cells and inhibit their viability through the induction of programmed death. Such effects of cadmium intoxication can be considered as a model of the impact of heavy metal pollution on vertebrates.


2017 ◽  
Vol 68 (7) ◽  
pp. 1506-1511
Author(s):  
Cerasela Mihaela Goidescu ◽  
Anca Daniela Farcas ◽  
Florin Petru Anton ◽  
Luminita Animarie Vida Simiti

Oxidative stress (OS) is increased in chronic diseases, including cardiovascular (CV), but there are few data on its effects on the heart and vessels. The isoprostanes (IsoP) are bioactive compounds, with 8-iso-PGF25a being the most representative in vivo marker of OS. They correlate with the severity of heart failure (HF), but because data regarding OS levels in different types of HF are scarce, our study was aimed to evaluate it by assessing the urinary levels of 8-iso-PGF2aand its correlations with various biomarkers and parameters. Our prospective study included 53 consecutive patients with HF secondary to ischemic heart disease or dilative cardiomyopathy, divided according to the type of HF (acute, chronic decompensated or chronic compensated HF). The control group included 13 hypertensive patients, effectively treated. They underwent clinical, laboratory - serum NT-proBNP, creatinine, uric acid, lipids, C reactive protein (CRP) and urinary 8-iso-PGF2a and echocardiographic assessment. HF patients, regardless the type of HF, had higher 8-iso-PGF2a than controls (267.32pg/�mol vs. 19.82pg/�mol, p[0.001). The IsoP level was directly correlated with ejection fraction (EF) (r=-0.31, p=0.01) and NT-proBNP level (r=0.29, p=0.019). The relative wall thickness (RWT) was negatively correlated with IsoP (r=-0.55, p[0.001). Also 8-iso-PGF25a was higher by 213.59pg/�mol in the eccentric left ventricular (LV) hypertrophy subgroup comparing with the concentric subgroup (p=0.014), and the subgroups with severe mitral regurgitation (MR) and moderate/severe pulmonary hypertension (PAH) had the highest 8-iso-PGF2a levels. Male sex, severe MR, moderate/severe PAH, high LV mass and low RWT values were predictive for high OS level in HF patients.Eccentric cardiac remodeling, MR severity and PAH severity are independent predictors of OS in HF patients.


2019 ◽  
Vol 70 (1) ◽  
pp. 78-83
Author(s):  
Alexandra Totan ◽  
Daniela Gabriela Balan ◽  
Daniela Miricescu ◽  
Radu Radulescu ◽  
Iulia Ioana Stanescu ◽  
...  

Oxidative stress (OS) plays an important role in NAFLD molecular mechanism. Nanoencapsulation represents a novel strategy to enhance therapeutic potential of conventional drugs. Our study analyses the encapsulated vitamin E effect on lipid metabolism and oxidative stress biomarkers in NAFLD rats. Animals were divided into 3 groups : G1 - the normal diet group; G2- the high caloric diet group ; G3 - high-caloric diet group receiving PLGA-vit E, 50 mg / kg. Serum advanced human oxidative protein (AOPP), total antioxidant capacity (TAC) and vitamin E were analysed using ELISA technique. Our results showed significant increase of G2 GPT, ALP, GGT, TG, glucose, TC and AOPP, versus G1 ( P [ 0.05) and a significant decrease of G2 serum TAC and vitamin E versus G1 results ( p = 0.01 and 0.01). Vitamin E nanoparticles (G3) caused a significant increase of TAC and significant decrease of serum AOPP, versus G2 (p [ 0.01). Results showed a significant reduction of GPT, GGT, ALP, TG and total cholesterol ( p [0.05) in G3 versus G2. PLGA nanoparticles should be considered an attractive and promising alternative to improve the bioavailability and biological activity of vitaminE.


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