The skin is the body’s biggest organ. You’ve undoubtedly heard this before, but most of us are less concerned with the specifics and more concerned with the appearance of our skin. After all, it’s our skin that remains one of the first things that others notice about us. We’d like to put our best face forward … literally. While most of us know the basics, such as keeping the skin clean and moisturizing regularly, any other specifics may or may not be as prominent in our lives or skincare routines. To help protect your skin and feel confident in yourself, take a look at why adding Vitamin E to the mix is a must.
The in vivo function of vitamin E is to scavenge peroxyl radicals via its phenolic (chromanol) hydroxyl group, thus protecting lipids against free radical-catalyzed peroxidation. The tocopheryl radical formed can then be reduced by reductants such as L-ascorbate. Other major products of α-tocopherol oxidation include α-tocopherylquinone and epoxy-α-tocopherols. The metabolites α-tocopheronic acid and its lactone, known as the Simon metabolites, are generally believed to be artefacts. In addition to these oxidation products, the other major class of tocopherol metabolites is the carboxyethyl-hydroxychromans (this pathway). These metabolites are produced in significant amounts in response to excess vitamin E ingestion.
A neuroprotective effect of dietary antioxidants on Parkinson’s disease (PD) risk has been suggested, but epidemiological evidence is limited.
To examine the associations between intake of dietary antioxidant vitamins and total antioxidant capacity and risk of PD.
We prospectively assessed the relationships of dietary antioxidant vitamins C and E, ß-carotene, and total antioxidant capacity with PD risk in two population-based cohorts (38,937 women and 45,837 men).
During a mean 14.9-year follow-up period, 1,329 PD cases were identified. Dietary intake of ß-carotene was associated with a lower risk of PD (hazard ratio: 0.86; 95% confidence interval: 0.78-0.95; Ptrend < 0.01 for women and hazard ratio: 0.91; 95% confidence interval: 0.84-0.99; Ptrend = 0.05 for men). An inverse association between dietary vitamin E and PD risk was found in women (hazard ratio: 0.87; 95% confidence interval: 0.79-0.96; Ptrend = 0.02). Dietary intake of vitamin C was inversely associated with PD risk in women at borderline significance (hazard ratio: 0.91; 95% confidence interval: 0.83-1.00; Ptrend = 0.04). There was no association between dietary total antioxidant capacity and PD risk in either women (hazard ratio: 0.93; 95% confidence interval: 0.84-1.02; Ptrend = 0.35) or men (hazard ratio: 1.00; 95% confidence interval: 0.93-1.07; Ptrend = 0.97).
Intake of dietary vitamin E and ß-carotene was associated with a lower risk of PD.
Currently, public pay more attention to the adverse effect of organophosphate pesticides on human and animal health and on the environment in developing nations. Vitamin E may protect the hepatocyte and increase the function of liver. The study was to investigate the effects of phoxim-induced hepatotoxicity on Sprague Dawley (SD) rats and the protection of vitamin E. SD rats received by gavage 180 mg kg-1 (per body weight) of phoxim, 200 mg kg-1 (per body weight) of vitamin E, and phoxim + vitamin E. The results showed that exposure to phoxim elevated liver coefficient; glutamyl transpeptidase (GGT), aspartate aminotransferase, alkaline phosphatase, total bilirubin, total bile acid, and alanine aminotransferase in the serum; ROS in the liver; and the expression of p53, Bax, CYP2E1, ROS, caspase-9, caspase-8, and caspase-3, while phoxim caused a reduction of total protein, albumin, and cholinesterase in the serum; acetylcholinesterase, total antioxidant capacity, glutathione peroxidase, and glutathione in the liver; and the expression of Bcl-2. Vitamin Emodified the phoxim-induced hepatotoxicity by reducing the GGT in the serum, malondialdehyde in the liver, and the expression of CYP2E1 significantly. There were no significant changes of globulin in the serum, the activity of catalase in the liver, as well as expression levels of Fas and Bad in the liver. Overall, subacute exposure to phoxim induced hepatic injury, oxidative stress damage, and cell apoptosis. Vitamin Emodified phoxim-induced hepatotoxicity slightly. And, vitamin E minimized oxidative stress damage and ultrastructural changes in rat hepatocytes notably.
Oxidative stress, in addition to the absence of the dystrophin protein, has been considered an important regulator of Duchenne muscular dystrophy (DMD). Vitamin E presents an important role as a potent antioxidant and in preserving the integrity of the cell membrane. In this study, we evaluated the effects of vitamin E therapy on some physiological pathways that can contribute to muscle injury in the diaphragm muscle of mdx mice (the experimental model of DMD) such as CK levels, inflammatory response, oxidative stress, and the enzymatic antioxidant system.
Mdx mice (14 d old) received 40 mg vitamin E/kg daily by oral gavage for 14 d, followed by the removal of the diaphragm muscle. Control mdx mice and C57BL/10 mice received saline only for the same period and were used as controls.
Vitamin E reduced the muscle fiber damage, oxidative stress, and inflammation process in the diaphragm muscle of mdx mice.
Vitamin E improves skeletal muscle injury in mdx mice, promoting membrane repair and exhibiting antioxidant and antiinflammatory effects. These vitamin E effects suggest that this antioxidant therapy may be a relevant approach for dystrophinopathies.
Oxidative stress is thought to play an important role in the pathogenesis of disorders associated with atherosclerosis. Alpha-tocopherol is considered to be an effective lipophilic antioxidant, which protects lipid membranes against peroxidation and thus prevents cell damage by reaction with free radicals. However, measurement of alpha-tocopherol concentration in serum does not reflect the content of α-tocopherol in membranes whereas erythrocyte alpha-tocopherol may be good indicator of antioxidative status. Therefore a simple isocratic reversed phase HPLC method has been developed and validated for the determination of alpha-tocopherol in human erythrocytes in a clinical setting. The content of alpha-tocopherol in human erythrocyte membrane and lipoperoxidation were studied in patients with severe hypercholesterolemia treated by lipoprotein apheresis. The group of hypercholesterolemic patients (n = 14) treated by lipoprotein apheresis was compared to healthy adult normolipidemic controls. After lipoprotein apheresis, the content of in membrane alpha-tocopherol did not change significantly despite decreased tocopherol in serum and lipoprotein fractions. We observed significantly decreased lipoperoxidation as revealed by serum TBARS, representing end products of lipid peroxidation, which increased from third day afterwards and remained significantly higher in comparison to controls until the next LDL-apheresis. We conclude that aggressive lipid lowering procedure with lipoprotein apheresis was associated with favorable transient decrease of lipoperoxidation. Simultaneously the cell membrane bound antioxidative defense mechanisms as reflected by the content of alpha-tocopherol in human erythrocyte membrane where not depressed in spite of its decreased plasma lipid carrier. Another variables involved remain to be investigated.
In a recently published study in The Journal of Nutrition, researchers examined the link between vitamin E intake and bone health in an animal model.
Vitamin E intake has recently been the focus of multiple bone health studies due to its reported beneficial effects. For this reason, scientists believe that vitamin E may be particularly helpful to individuals who consume a high-fat diet since excess body fat is associated with decreased bone density and thus, a higher likelihood of developing osteoporosis. Additionally, several animal studies have demonstrated that a high-fat diet, which causes oxidative stress, significantly impairs bones’ structural and mechanical properties. Although some studies have shown beneficial effects of Vitamin E, a known antioxidant, other studies have suggested that Vitamin E may have negative effects on bone health.
Tocotrienols are forms of vitamin E that are present in several important food crops. Compared to tocopherols, less research has been conducted on these compounds because of their low bioavailability and distribution in plant tissues. Both tocotrienols and tocopherols are known for their antioxidant and anticancer activities, which are beneficial for both humans and animals. Moreover, tocotrienols possess certain properties which are not found in tocopherols, such as neuroprotective and cholesterol-lowering activities. The contents of tocotrienolsin plants vary. Tocotrienols constitute more than 70% and tocopherols less than 30% of the total vitamin E content in palm oil, which is the best source of vitamin E. Accumulation of tocotrienols also occurs in non-photosynthetic tissues, such as the seeds, fruits and latex of some monocotyledonous and dicotyledonous plant species. The use of biotechnological techniques to increase the tocotrienol content in plants, their biological functions, and benefits to human health are discussed in this review.
The School of Biological Sciences, Faculty of Science, the University of Hong Kong (HKU), in collaboration with the Institut de Biologie Moléculaire des Plantes (CNRS, Strasbourg, France), has identified a new strategy to simultaneously enhance health-promoting vitamin E by ~6-fold and double both provitamin A and lycopene contents in tomatoes, to significantly boost antioxidant properties.
An experimental “golden” potato could hold the power to prevent disease and death in developing countries where residents rely heavily upon the starchy food for sustenance, new research suggests.
A serving of the yellow-orange lab-engineered potato has the potential to provide as much as 42 percent of a child’s recommended daily intake of vitamin A and 34 percent of a child’s recommended intake of vitamin E, according to a recent study co-led by researchers at The Ohio State University.