α-Tocopherol is a lipid-soluble antioxidant that is specifically required for reproduction and embryogenesis. However, since its discovery, α-tocopherol's specific biologic functions, other than as an antioxidant, and the mechanism(s) mediating its requirement for embryogenesis, remain unknown. As an antioxidant, α-tocopherol protects polyunsaturated fatty acids (PUFAs) from lipid peroxidation. α-Tocopherol is likely required during embryonic development to protect PUFAs that are crucial to development, specifically arachidonic (ARA) and docosahexaenoic (DHA) acids. Additionally, ARA and DHA are metabolized to bioactive lipid mediators via lipoxygenase enzymes and α-tocopherol may directly protect, or it may mediate the production and/or actions of these lipid mediators. In this review, we discuss how α-tocopherol 1) prevents the nonspecific, radical-mediated peroxidation of PUFAs, 2) functions within a greater antioxidant network to modulate the production and/or function of lipid mediators derived from 12- and 12/15-lipoxygenase and 3) modulates 5-lipoxygenase activity. The application and implication of such interactions with be discussed in the context α-tocopherol requirements during embryogenesis.
"This ascorbate-tocopherol-GSH antioxidant system is selfregenerating at the expensive of energy (NADH, NADPH). Maintenance of this antioxidant network is crucial to protect cellular membranes against radical-mediated degradation (Lebold and Traber 2014). Cells have evolved adaptive mechanisms to endure oxidative stress. "
[Show abstract][Hide abstract] ABSTRACT: ARTICLE INFO ABSTRACT The eyes are at particular risk for oxidative damage due to their high exposure to oxygen, a large amount of fatty acids in the retina and also high light exposure, environmental pollutants and ultraviolet rays. Oxidative stress to the largely retinal pigment epithelial cell layer (RPE) over time is reported to produce tissue dysfunction that contributes to the development of the pathogenesis of many diseases of the visual apparatus. The present paper discussed the evidence found about the possible role of oxidative damage in the pathogenesis of several eye diseases (glaucoma, cataract, diabetic retinopathy, macular degeneration) and the role of diet and antioxidant supplements in the prevention and treatment of such diseases. In recent years it has been suggested that free radicals and oxidative stress are part of this process, which fact is confirmed in many instances, it has been shown that the use of exogenous antioxidants preventive or stimulation of endogenous antioxidant systems retard appearance of the main signs and symptoms of ocular pathologies. INTRODUCATION Biological redox (reduction/oxidation) reactions remain poorly understood despite their importance to most normal physiological and many pathophysiological processes (Sarsour et al., 2009; Valko et al., 2007) Intracellular redox status, which refers to the ratio of the reversible oxidized form to the reduced form of a specific redox couple, maintains cellular homeostasis through the balance of oxidants and antioxidants. Redox reactions normally regulate vascular tone (Faraci et al., 2006), platelet activation (Freedman et al., 2008), and the immune response (Forman and Torres et al., 2002). When redox homeostasis is compromised and chronic oxidative stress persists the pathophysiological consequences involving the cardiovascular, pulmonary, renal, gastrointestinal, hepatic, and neurologic systems, as well as metabolic and inflammatory diseases. Oxidative stress can be defined as a state of imbalance toward the factors that generate reactive
"Dunn-Thomas reported that vitamin E could influence retinal precursor cell differentiation by reducing stress-related function . These studies of vitamin E have primarily utilized ␣-tocopherol, as it exerts the highest biological activity . However, recent studies have suggested that ␦-tocopherol may be more effective. "
[Show abstract][Hide abstract] ABSTRACT: The effects of the vitamin E isomer δ-tocopherol on neural stem cell (NSC) differentiation have not been investigated until now. Here we investigated the effects of δ-tocopherol on NSC neural differentiation, maturation and its possible mechanisms. Neonatal rat NSCs were grown in suspended neurosphere cultures, and were identified by their expression of nestin protein and their capacity for self-renewal. Treatment with a low concentration of δ-tocopherol induced a significant increase in the percentage of β-III-tubulin-positive cells. δ-Tocopherol also stimulated morphological maturation of neurons in culture. We further observed that δ-tocopherol stimulation increased the expression of voltage-dependent Ca2+ channels. Moreover, a L-type specific Ca2+ channel blocker verapamil reduced the percentage of differentiated neurons after δ-tocopherol treatment, and blocked the effects of δ-tocopherol on NSC differentiation into neurons. Together, our study demonstrates that δ-tocopherol may act through elevation of L-type calcium channel activity to increase neuronal differentiation.
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