Oliver H. Emerson

Bio: Oliver H. Emerson is an academic researcher from University of California, Berkeley. The author has contributed to research in topics: Vitamin E & alpha-Tocopherol. The author has an hindex of 8, co-authored 19 publications receiving 559 citations.

The Isolation from Wheat Germ Oil of an Alcohol, α-Tocopherol, Having the Properties of Vitamin E

Abstract: We have prepared from the non-saponifiable matter of wheat germ oil thress aflophanates: 1. M.p. 250°. This is a possibly the allophante of β-amyrin. The alcohol regenrated from the allopohante has no vitamin E potency. 2. M.p. 138°, readily crystallizing in long needles. The analysis agree with values required by monollophantes of an alcohol, C39H50O2. The alcohol from this allophante apparenelly has some vitamin E potency, but less than that from the third allophanate. 3. M.p. 158-160°. From this allophanate, the alcohol—for which we propose the name α-tocopherol—when given in a single dose of 3 mg. always enables vitamin E-deficient rats to bear young. α-Tocopherol shows a characteristic absoption band at 2980 A., E1 per cent1 cm. = 90 ca. Treatment with methyl alcoholic silver nitrate converts it to a substance which has absorption bands at 2710 and 2620 A respectively, E1 per centcm. = 480 ca., and possesses and some vitamin E activity. α-Tocopherol yields a crystaline p-nitrophenylurethane melting at 120-131°. Analyses of both the urethane and the allophanate indicate a provisional formula for α-tocopherol of C29H50O2

VITAMIN E: Interactions With Free Radicals and Ascorbate

Abstract: The association of the tocopherols with lipid peroxidation in biological systems began in the early days of investigations on the chemical nature of these substances (25). Since then a great deal of work has attempted to relate the symptoms of vitamin E deficiency with peroxidative degradation of lipids, primarily those associated with membranous organelles. The signs of vitamin E deficiency in various species of animals are diverse, involving different tissues with different manifestations and different degrees of severity. Thus, it seems clear that the biological function of this vitamin is not specific in the sense of its being a cofactor for an enzymic reaction (as is the case for the B-complex vitamins). Given the appropriate species and certain dietary and environmental conditions, essentially any tissue can be made to develop characteristic signs as a result of a deficiency of this vitamin. In some human disease states, supple­ mentation of vitamin E at levels far exceeding those normally required amelio­ rates or improves the condition. Because of this multiplicity of effects, a common denominator that might explain the effects of a deficiency or excess of this vitamin is not obvious. A common denominator to consider, however, is

Chlorogenic Acid, Quercetin-3-Rutinoside and Black Tea Phenols Are Extensively Metabolized in Humans

Abstract: Dietary phenols are antioxidants, and their consumption might contribute to the prevention of cardiovascular disease. Coffee and tea are major dietary sources of phenols. Dietary phenols are metabolized extensively in the body. Lack of quantitative data on their metabolites hinders a proper evaluation of the potential biological effects of dietary phenols in vivo. The aim of this study was to identify and quantify the phenolic acid metabolites of chlorogenic acid (major phenol in coffee), quercetin-3-rutinoside (major flavonol in tea) and black tea phenols in humans, and determine the site of metabolism. Healthy humans (n = 20) with an intact colon participated in a dietary controlled crossover study, and we identified and quantified ∼60 potential phenolic acid metabolites in urine. Half of the ingested chlorogenic acid and 43% of the tea phenols were metabolized to hippuric acid. Quercetin-3-rutinoside was metabolized mainly to phenylacetic acids, i.e., 3-hydroxyphenylacetic acid (36%), 3-methoxy-4-hydroxyphenylacetic acid (8%) and 3,4-dihydroxyphenylacetic acid (5%). In contrast, in seven humans without a colon, we found only traces of phenolic acid metabolites in urine after they had ingested chlorogenic acid and quercetin-3-rutinoside. This implies that the colonic microflora convert most of these dietary phenols into metabolites that then reach the circulation. Metabolites of dietary phenols have lower antioxidant activity than their parent compounds; therefore, the contribution of dietary phenols to antioxidant activity in vivo might be lower than expected from in vitro tests.

The antioxidant effects of thylakoid Vitamin E (α-tocopherol)

Abstract: Vitamin E (α-tocopherol) is essential for the prevention of photo-oxidative deterioration of biomembranes. The occurrence, relative biological activity and distribution of tocopherols in photosynthetic membranes is considered together with the possible biochemical and biophysical mechanisms by which tocopherols confer protection upon illuminated membranes. The common protective effects of Vitamin E in photo-synthetic membranes and in medically important light-induced diseases and conditions of the skin and eye in animal cell membranes are discussed. The importance of the Vitamin E-Vitamin C thylakoid antioxidant system is also examined, in terms of susceptibility to photo-oxidative damage under stress conditions including chilling, ageing and senescence, drought, atmospheric pollutants, herbicides and photosensitizing fungal toxins.

Ubiquinone biosynthesis in microorganisms

Abstract: The quinoid nucleus of the benzoquinone, ubiquinone (coenzyme Q; Q), is derived from the shikimate pathway in bacteria and eukaryotic microorganisms. Ubiquinone is not considered a vitamin since mammals synthesize it from the essential amino acid tyrosine. Escherichia coli and other Gram-negative bacteria derive the 4-hydroxybenzoate required for the biosynthesis of Q directly from chorismate. The yeast, Saccharomyces cerevisiae, can either form 4-hydroxybenzoate from chorismate or tyrosine. However, unlike mammals, S. cerevisiae synthesizes tyrosine in vivo by the shikimate pathway. While the reactions of the pathway leading from 4-hydroxybenzoate to Q are the same in both organisms the order in which they occur differs. The 4-hydroxybenzoate undergoes a prenylation, a decarboxylation and three hydroxylations alternating with three methylation reactions, resulting in the formation of Q. The methyl groups for the methylation reactions are derived from S-adenosylmethionine. While the prenyl side chain is formed by the 2-C-methyl-D-erythritol 4-phosphate (non-mevalonate) pathway in E. coli, it is formed by the mevalonate pathway in the yeast.

Molecular mechanisms of vitamin e transport

Abstract: If the function of vitamin E is that of an antioxidant and the various forms of vitamin E have similar antioxidant activities, then why does RRR-alpha-tocopherol have the highest biologic activity? This chapter describes how interactions by investigators from various scientific disciplines using stable isotopes, molecular biology tools, and sophisticated genetic studies of humans with vitamin E deficiency have led to an understanding of this problem. This chapter provides an overview of (a) studies using deuterated tocopherols that demonstrated that the plasma preference for alpha-tocopherol is dependent on metabolic processes in the liver; (b) the isolation, molecular biology, and function of the alpha-tocopherol transfer protein; and (c) studies that demonstrated that patients who were vitamin E deficient as a result of no known cause had defective alpha-tocopherol transfer protein genes. Finally, we focus on the future--what remains to be learned about the regulation of vitamin E in tissues.