Antioxidant Function and Health Implications of Vitamin E

Abstract

Superoxide, a key precursor of important reactive oxygen/nitrogen species (ROS/RNS), may release iron from its protein complex. By mediating the generation and/level of superoxide, vitamin E, the most important fat-soluble antioxidant and free radical scavenger, may exert its antioxidant function by limiting the formation of reactive hydroxyl radicals and peroxynitrite. The antioxidant function of vitamin E is augmented by GSH peroxidase and related metabolic systems which respond adaptively and compensatively to oxidative stress. By mediating the levels of ROS/RNS, vitamin E may also modulate the activation and/or expression of redox-sensitive biological response modifiers, and thereby attenuate the cellular events leading to the onset and development of aging and other degenerative disorders. Earlier epidemiological data and retrospective studies show an association between increased intake of vitamin E and reduced risk of cardiovascular disease, cancer, and other disorders. However, subsequent prospective randomized placebo-controlled studies and interventional trials have provided inconsistent findings. Data available from recent large-scale interventional trials suggest that vitamin E supplements at high doses are not beneficial.Keywords: Vitamin E, tocopherols, superoxide, biological function, health benefit. INTRODUCTIONVitamin E is referred to all tocol (tocopherol) and tocotrienol derivatives qualitatively exhibiting the biological activity of RRR-α-tocopherol. There are four tocopherols (α-, β-, γ-and δ-) and four tocotrienols (α-, β-, γ-and δ-) that occur naturally, differing in the number and position of methyl groups on the chroman ring [1,2]. Vitamin E was discovered 90 years ago, and a number of species-dependent and organ-specific deficiency symptoms of vitamin E were reported later [3,4]. However, due to the lack of clinically defined deficient syndromes attributable to vitamin E and the difficult to produce vitamin E deficiency in adults, its essentiality for humans was established only after the discovery of α-tocopherol transfer protein decades later [2,[5][6][7][8]. The transfer protein binds RRR-α-tocopherol preferentially over other forms/isomers of tocopherols, and enhances its transfer and return to the liver. The presence of α-tocopherol transfer protein is largely responsible for higher biological activity of RRR-α-form than other forms/isomers.

Copper: toxicological relevance and mechanisms

“…Cu overload also reduces the activity of cytochrome c oxidase and impairs liver mitochondrial respiration (Myers et al, 1993), and increase in rat liver chemiluminescence, while the activities of catalase and GSH peroxidase are significantly decreased (Ossola et al, 1997). By overwhelming body antioxidant systems and inducing DNA damage, lipid peroxidation, protein modification and other effects, ROS may lead to the development of degenerative diseases, including cancer, cardiovascular disease, diabetes, atherosclerosis, neurological disorders and chronic inflammation (Chow, 1979; Chow and Chow-Johnson, 2013; Jomova and Valko, 2011). …”

“…As a number of biological response modifiers are redox-sensitive, intracellular production/level of ROS may alter the expression and activation of vital biological modifiers, which in turn may alter cell proliferation, differentiation, apoptosis, and other cellular events (D’Autréaux and Toledano, 2007; Chow and Chow-Johnson, 2013; Long et al, 2014; Caliceti et al, 2014). Therefore, Cu-induced changes in the redox properties may alter neurotransmitter biosynthesis, angiogenesis and other physiological processes.…”

Pengaruh suplementasi vitamin e (α-tokoferol) terhadap kadar gamma glutamil transferase (ggt) dan kadar nitric oxide (no) pada tikus (Studi pada tikus rattus novergicus strain wistar jantan terpapar inhalasi uap benzene)

“…Vitamin E juga mengurangi besi labil sebagai penyebab kerusakan oksidatif. (29) Selain itu vitamin E diduga memiliki efek protektif terhadap glutathion. (30) Suplementasi vitamin E meningkatkan konsentrasi glutathion seluler, karena vitamin E dapat memodulasi konsentrasi glutathion.…”

“…Peran vitamin E dalam penelitian ini diduga dapat mengurangi besi labil yang menyebabkan kerusakan oksidatif. (29) Vitamin E menghambat pembentukan superoksida dan akhirnya mengurangi hidroksil reaktif dan peroksinitrit dengan menyumbangkan hidrogen dari gugus hidroksil (OH -) ke radikal bebas dan membuat mereka tidak aktif serta efek protektif terhadap glutathion. (30) Hal ini akan memperbaiki status antioksidan dan juga mengurangi jumlah besi labil mengarah pada penurunan stres oksidatif (penurunan kadar GGT) yang akan diikuti dengan penurunan ekpresi iNOS menghasilkan NO terhadap induksi radikal bebas dan produksi NO dari GSNO.…”

Physiological and Pathological Roles of Free Radicals in Male Reproduction

“…The molecular functions fulfilled specifically by α-tocopherol have yet to be fully described; however, the antioxidant feature is the flagship of the biological activity related to vitamin E [128].…”