VITAMIN E SUPPLEMENTATION - EFFECT ON OXIDATIVE DAMAGE INDUCED BY PROLONGED PHYSICAL EXERCISE 226

We previously reported that, in rodents, a diet with a high oxidised frying oil (OFO) content leads to glucose intolerance associated with a reduction in insulin secretion. The present study aimed at investigating the impairment of pancreatic islets caused by dietary OFO. C57BL/6J mice were divided into three groups to receive a low-fat basal diet containing 5 g/100 g of fresh soyabean oil (LF group) or a high-fat diet containing 20 g/100 g of either fresh soyabean oil (HF group) or OFO (HO group). After 8 weeks, mice in the HO group showed glucose intolerance and hypoinsulinaemia, and their islets showed impaired glucose-stimulated insulin secretion (P < 0·05; HO group v. LF and HF groups). Significantly higher oxidative stress and a lower mitochondrial membrane potential were observed in the islets in the HO group compared with the LF and HF groups. Immunoblots showed that the reduction in insulin levels in HO islets was associated with activation of the c-Jun NH2-terminal kinase and a reduction in levels of pancreatic and duodenal homeobox factor-1. In a second study, when dietary OFO-induced tissue vitamin E depletion was prevented by large-dose vitamin E supplementation (500 IU(1·06 mmol all-rac-α-tocopherol acetate)/kg diet; HO+E group), the OFO-mediated reduction in islet size and impairment of glucose tolerance and insulin secretion were significantly attenuated (P < 0·05; HO group v. HO+E group). We conclude that a high level of dietary OFO ingestion impairs glucose metabolism by causing oxidative damage and compromising insulin secretion in pancreatic islets, and that these effects can be prevented by vitamin E supplementation.

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Vitamin E Supplementation and Mitochondria in Experimental and Functional Hyperthyroidism: A Mini-Review

Nutrients ◽

10.3390/nu11122900 ◽

2019 ◽

Vol 11 (12) ◽

pp. 2900 ◽

Cited By ~ 3

Author(s):

Gaetana Napolitano ◽

Gianluca Fasciolo ◽

Sergio Di Meo ◽

Paola Venditti

Keyword(s):

Vitamin E ◽

Oxidative Damage ◽

Cell Function ◽

Peroxyl Radicals ◽

Antioxidant Vitamin ◽

Mitochondrial Ros ◽

Mitochondrial Population ◽

Vitamin E Supplementation ◽

Lipid Soluble Antioxidant

Mitochondria are both the main sites of production and the main target of reactive oxygen species (ROS). This can lead to mitochondrial dysfunction with harmful consequences for the cells and the whole organism, resulting in metabolic and neurodegenerative disorders such as type 2 diabetes, obesity, dementia, and aging. To protect themselves from ROS, mitochondria are equipped with an efficient antioxidant system, which includes low-molecular-mass molecules and enzymes able to scavenge ROS or repair the oxidative damage. In the mitochondrial membranes, a major role is played by the lipid-soluble antioxidant vitamin E, which reacts with the peroxyl radicals faster than the molecules of polyunsaturated fatty acids, and in doing so, protects membranes from excessive oxidative damage. In the present review, we summarize the available data concerning the capacity of vitamin E supplementation to protect mitochondria from oxidative damage in hyperthyroidism, a condition that leads to increased mitochondrial ROS production and oxidative damage. Vitamin E supplementation to hyperthyroid animals limits the thyroid hormone-induced increases in mitochondrial ROS and oxidative damage. Moreover, it prevents the reduction of the high functionality components of the mitochondrial population induced by hyperthyroidism, thus preserving cell function.

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Vitamin E, Physical Exercise and Tissue Oxidative Damage

Ciba Foundation Symposium 101 - Biology of Vitamin E - Novartis Foundation Symposia ◽

10.1002/9780470720820.ch5 ◽

2008 ◽

pp. 56-69 ◽

Cited By ~ 2

Author(s):

A. T. Quintanilha ◽

L. Packer

Keyword(s):

Vitamin E ◽

Physical Exercise ◽

Oxidative Damage

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Effects of low-volume walking programme and vitamin E supplementation on oxidative damage and health-related variables in healthy older adults

Nutrition & Metabolism ◽

10.1186/1743-7075-10-38 ◽

2013 ◽

Vol 10 (1) ◽

pp. 38 ◽

Cited By ~ 4

Author(s):

Jong-Hwan Park ◽

Masashi Miyashita ◽

Masaki Takahashi ◽

Noriaki Kawanishi ◽

Seong-Ryu Bae ◽

...

Keyword(s):

Older Adults ◽

Vitamin E ◽

Oxidative Damage ◽

Healthy Older Adults ◽

Health Related ◽

Low Volume ◽

Walking Programme ◽

Vitamin E Supplementation

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Protective effect of vitamin E on exercise-induced oxidative damage in young and older adults

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1993.264.5.r992 ◽

1993 ◽

Vol 264 (5) ◽

pp. R992-R998 ◽

Cited By ~ 16

Author(s):

M. Meydani ◽

W. J. Evans ◽

G. Handelman ◽

L. Biddle ◽

R. A. Fielding ◽

...

Keyword(s):

Vitamin E ◽

Oxidative Damage ◽

Protective Effect ◽

Eccentric Exercise ◽

Conjugated Dienes ◽

Alpha Tocopherol ◽

Double Blind ◽

Tocopherol Concentration ◽

Exercise Induced ◽

Vitamin E Supplementation

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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Fish oil and vitamin E supplementation in oxidative stress at rest and after physical exercise

Journal of Applied Physiology ◽

10.1152/jappl.1997.83.1.189 ◽

1997 ◽

Vol 83 (1) ◽

pp. 189-195 ◽

Cited By ~ 43

Author(s):

Chandan K. Sen ◽

Mustafa Atalay ◽

Jyrki Ågren ◽

David E. Laaksonen ◽

Sashwati Roy ◽

...

Keyword(s):

Oxidative Stress ◽

Lipid Peroxidation ◽

Vitamin E ◽

Physical Exercise ◽

Fish Oil ◽

Protein Oxidation ◽

Protein Carbonyl ◽

Oxidative Protein Damage ◽

Exercise Induced ◽

Vitamin E Supplementation

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.

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