Influence of Alpha-Tocopherol (Vitamin E) on Storage Stability of Raw Pork and Bacon

1980 ◽  
Vol 43 (4) ◽  
pp. 265-267 ◽  
Author(s):  
J. BUCKLEY ◽  
F. CONNOLLY

Feeding supplemental Vitamin E to pigs before slaughter has a beneficial effect on the storage stability of pork during refrigerated and frozen storage, particularly if packaged in non-vacuum packages. The effects of Vitamin E supplementation on bacon are not as pronounced.

1999 ◽  
Vol 8 (1) ◽  
pp. 9-18 ◽  
Author(s):  
K. SUOMI ◽  
K. PARTANEN ◽  
T. ALAVIUHKOLA

A 2 × 4 factorial experiment was conducted with 80 growing-finishing pigs to evaluate effects of barley storage (stored barley harvested the previous year or freshly harvested barley) and supplemental vitamin E (0, 40, 80 or 160 mg/kg as all-rac-a-tocopheryl acetate) on pig performance and the storage stability and eating quality of frozen pork. Pigs were fed isoenergetic barley-soybean meal diets and vitamin E was rationed on the top of feed, a 2-d dose at a time. Stored and freshly harvested barley contained 33.5 and 31.2 mg/kg of vitamin E in the beginning and 33.0 and 38.7 mg/kg at the end of the study, respectively. Supplemental vitamin E had a quadratic effect on pig growth (P < 0.05), the greatest weight gains being observed with 40 mg/kg of supplemental vitamin E in both barley diets. Vitamin E supplementation increased linearly serum (P < 0.001) and quadratically back fat a-tocopherol (P < 0.01). Plasma gluthathione peroxidase activity increased as pigs grew older (P < 0.001), and at slaughter it decreased linearly with supplemental vitamin E (P < 0.05). Dietary vitamin E supplementation did not affect the content of thiobarbituric acid reactive substances (TBARS) or the organoleptic quality of pork stored frozen (-18°C) for 16 weeks. The TBARS content of pork increased with time (0 to 8 d) thawed meat was displayed under fluorescent light at 8°C (P < 0.001) which was detected as a poorer taste. In conclusion, supplemental dietary vitamin E above 40 mg/kg feed does not improve pig performance nor the storage stability or eating quality of frozen pork when freshly harvested or stored barley from good harvest conditions is fed to growing-finishing pigs.;


1996 ◽  
Vol 270 (2) ◽  
pp. G376-G384 ◽  
Author(s):  
S. Parkkila ◽  
O. Niemela ◽  
R. S. Britton ◽  
K. E. Brown ◽  
S. Yla-Herttuala ◽  
...  

Hepatic iron overload can cause lipid peroxidation with the formation of aldehydic products, hepatocellular injury, and fibrosis. Vitamin E (alpha-tocopherol) may prevent peroxidation-induced hepatic damage. We used confocal laser scanning microscopy, digital image analysis, and immunohistochemical methods to quantitate aldehyde-derived peroxidation products in the liver of rats with experimental iron overload with or without supplemental vitamin E. A strong autofluorescent reaction colocalizing with iron deposits was present in the livers of iron-loaded rats. Fluorescent granules were unevenly distributed in the cytosol of both hepatocytes and Kupffer cells in the periportal regions. Immunohistochemical studies revealed the presence of malon-dialdehyde adducts in the periportal regions of the ironloaded rats. Vitamin E supplementation markedly reduced the fluorescence intensity and the amount of aldehyde-derived peroxidation products and changed the distribution of stainable iron and iron-associated peroxidation products such that their levels were much decreased in Kupffer cells. These results indicate that aldehyde-derived covalent chemical addition products are formed in the liver in iron overload. Vitamin E supplementation markedly reduces the amount of these compounds and changes their cellular distribution. These findings should be implicated in the role of antioxidant therapy in conditions causing iron overload and lipid peroxidation.


2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 1810-1810
Author(s):  
Jiaqi Huang ◽  
Stephanie Weinstein ◽  
Wendy Mack ◽  
Howard Hodis ◽  
Demetrius Albanes

Abstract Objectives Vitamin E is an essential micronutrient and critical human antioxidant that has been tested for cancer and cardiovascular preventative effects for decades with conflicting results. For example, prostate cancer incidence was reduced by a low-dose vitamin E supplement in the Alpha-Tocopherol, Beta-Carotene Cancer Prevention (ATBC) Study, but the findings were not replicated by high-dose vitamin E trials such as the Selenium and Vitamin E Cancer Prevention Trial (SELECT). The present investigation examined the serum metabolomic responses to low- and high-dose vitamin E supplementation in order to gain biological insight into the divergent trial outcomes. Methods We examined baseline and on-study serum samples for 154 men randomly assigned to receive 400 IU vitamin E (as alpha-tocopheryl acetate; ATA) or placebo daily in the Vitamin E Atherosclerosis Prevention Study (VEAPS), and 100 men administered 50 IU ATA or placebo daily in the ATBC Study. Over 970 known metabolites were identified using an ultrahigh-performance LC-MS/MS platform. Linear regression models estimated the change in serum metabolites of men supplemented with vitamin E to those assigned to placebo in VEAPS compared with ATBC. Results Serum alpha-carboxyethyl hydrochroman (CEHC) sulfate, alpha-tocopherol, and beta-/gamma-tocopherol were significantly altered by supplementation with ATA in both the VEAPS and ATBC trials (all P-values ≤ 5.1 × 10−5, the Bonferroni multiple-comparisons corrected statistical threshold). Serum C22 lactone sulfate was also significantly decreased in response to the high-dose vitamin E supplement in VEAPS (β = −0.70, P-value = 8.1 × 10−6), but not altered in the low-dose ATBC trial (β = −0.17, P-value = 0.4). Additionally, changes in several androgenic steroid metabolites were strongly related to the vitamin E supplement-associated change in C22 lactone sulfate only in the high-dose VEAPS trial. Conclusions We found evidence of a dose-dependent vitamin E supplementation effect on a novel C22 lactone sulfate compound as well as several androgenic steroids that may have relevance to previous controlled trial findings for prostate cancer. Funding Sources This research was supported by the Intramural Research Program of the National Cancer Institute, National Institutes of Health, U.S. Public Health Service, Department of Health and Human Services.


1982 ◽  
Vol 47 (1) ◽  
pp. 53-60 ◽  
Author(s):  
David S. Muduuli ◽  
Ronald R. Marquardt ◽  
Wilhelm Guenter

1. Experiments were conducted to study the effects of dietary vicine (2, 6-diamino-4, 5 dihydroxy pyrimidine-5 (β-D-glucopyranoside)) and supplemental vitamin E on the performance of laying hens and growing chicks.2. Chicks fed on diets that contained vicine had similar growth rates but slightly higher levels of spontaneous haemolysis of erythrocytes than birds fed on a control diet.3. Vicine when fed to laying hens had a very dramatic effect. It depressed food consumption, egg weight, fertility and hatchability of eggs, packed cell volume and erythrocyte haemoglobin levels and led to increased liver weights, liver glutathione levels, liver and plasma lipid levels, plasma lipid peroxide levels and erythrocyte haemolysis in vitro. Liver protein and plasma vitamin E:lipid levels were not altered. Vitamin E supplementation slightly increased egg weights, markedly improved fertility and hatchability of eggs and lowered liver weights and lipid levels but did not affect the other factors examined.4. It is concluded that vicine which was isolated from faba beans (Vicia faba L.) has a marked influence on the metabolism of the laying hen and only a slight effect on the growing chick. Vicine or its metabolites or both cause peroxidation of cellular components which result in abnormal lipid transport or synthesis or both, increased fragility of erythrocytes, and reduced fertility. These effects are overcome to varying extents by supplemental vitamin E.


2016 ◽  
Vol 116 (9) ◽  
pp. 1530-1536 ◽  
Author(s):  
Harri Hemilä

AbstractAnalyses in nutritional epidemiology usually assume a uniform effect of a nutrient. Previously, four subgroups of the Alpha-Tocopherol, Beta-Carotene Cancer Prevention (ATBC) Study of Finnish male smokers aged 50–69 years were identified in which vitamin E supplementation either significantly increased or decreased the risk of pneumonia. The purpose of this present study was to quantify the level of true heterogeneity in the effect of vitamin E on pneumonia incidence using the I2 statistic. The I2 value estimates the percentage of total variation across studies that is explained by true differences in the treatment effect rather than by chance, with a range from 0 to 100 %. The I2 statistic for the effect of vitamin E supplementation on pneumonia risk for five subgroups of the ATBC population was 89 % (95 % CI 78, 95 %), indicating that essentially all heterogeneity was true variation in vitamin E effect instead of chance variation. The I2 statistic for heterogeneity in vitamin E effects on pneumonia risk was 92 % (95 % CI 80, 97 %) for three other ATBC subgroups defined by smoking level and leisure-time exercise level. Vitamin E decreased pneumonia risk by 69 % among participants who had the least exposure to smoking and exercised during leisure time (7·6 % of the ATBC participants), and vitamin E increased pneumonia risk by 68 % among those who had the highest exposure to smoking and did not exercise (22 % of the ATBC participants). These findings refute there being a uniform effect of vitamin E supplementation on the risk of pneumonia.


Circulation ◽  
2018 ◽  
Vol 137 (suppl_1) ◽  
Author(s):  
Susanne Rautiainen ◽  
J. Michael Gaziano ◽  
William G Christen ◽  
Vadim Bubes ◽  
Gregory Kotler ◽  
...  

Background: Large-scale trials have not supported a role of vitamin E supplementation in reducing the risk of cardiovascular disease (CVD). We investigated whether baseline diet quality and vitamin E intake modified the effect of randomized vitamin E supplementation on the risk of CVD in the Physicians’ Health Study II (PHS II). Methods: The PHS II was a randomized, double-blind, placebo-controlled trial testing 400 IU synthetic α-tocopherol on alternate days. 14,641 men aged ≥50 years were included. 13,316 men (91%) completed a 116-item food frequency questionnaire and were included in our intention-to-treat analysis. We examined effect modification by baseline diet quality as assessed by dietary patterns (tertiles of the Alternate Healthy Eating Index [AHEI] and Alternate Mediterranean Diet [AMED]), and by dietary and supplemental vitamin E intake. Results: During a mean 8.0 years of follow-up, baseline diet quality or vitamin E intake did not modify the effect of vitamin E use on the primary endpoint of major CVD events ( Table ). However, AHEI modified the effect of randomized vitamin E use on the secondary endpoint of MI (P, interaction=0.02), with a statistically significant 39% lower risk among men in the lowest tertile of the AHEI. A similar and statistically significant 37% lower risk of MI was observed in the lowest category of the AMED (P, interaction=0.08). There was no evidence that diet quality modified the effect of vitamin E use on risks of stroke or CVD mortality, and baseline dietary and supplemental vitamin E intake did not modify the effects on any outcome. Conclusion: Diet quality did not modify the effect of vitamin E supplementation on most CVD outcomes but did modify its effect on MI. Given concerns about multiple comparisons and the need for replication, our findings should be interpreted with caution.


1993 ◽  
Vol 264 (5) ◽  
pp. R992-R998 ◽  
Author(s):  
M. Meydani ◽  
W. J. Evans ◽  
G. Handelman ◽  
L. Biddle ◽  
R. A. Fielding ◽  
...  

The protective effect of vitamin E supplementation on exercise-induced oxidative damage was tested in 21 male volunteers. Nine young (22-29 yr) and 12 older (55-74 yr) sedentary male subjects participated in a double-blind protocol and received either 800 IU dl-alpha-tocopherol or a placebo daily. After 48 days, vitamin E supplementation significantly increased alpha-tocopherol in plasma and skeletal muscle. Subjects then performed a bout of eccentric exercise at 75% of their maximum heart rate by running down an inclined treadmill for 45 min. All vitamin E-supplemented subjects excreted less (P < 0.05) urinary thiobarbituric acid adducts after the exercise bout than placebo subjects at 12 days postexercise (35 and 18% above baseline in young and old supplemented groups, respectively, vs. 60 and 80% in young and old placebo groups, respectively). After exercise, the initial difference in alpha-tocopherol concentration of muscle between young placebo and vitamin E-supplemented groups was diminished and muscle lipid conjugated dienes tended to increase (P = 0.09) in placebo subjects. Placebo subjects had a significant decrease in major fatty acids of muscle biopsy taken immediately after exercise. When normalized for the hemoconcentration effects of exercise, the plasma concentration of vitamins E and C and uric acid showed no significant change. The alterations in fatty acid composition, vitamin E, and lipid conjugated dienes in muscle and in urinary lipid peroxides in controls after eccentric exercise are consistent with the concept that vitamin E provides protection against exercise-induced oxidative injury.


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