Role of Ascorbic Acid in Microsomal Electron Transport and the Possible Relationship to Hydroxylation Reactions

Staudinger, H.; Krisch, K; Leonhäuser, S.

doi:10.1111/j.1749-6632.1961.tb46119.x

Cited by 72 publications

(8 citation statements)

References 20 publications

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“…Vitamin C is a well known component related to the control of oxido-reduction states of living cell, but detailed role of vitamin C has not been fully elucidated (27 (30) reported that the hydroxylation of acetanilide, hexobarbital and zoxazolamine was decreased in vitamin C deficient guinea-pigs. However, the studies on the mechanism of decreased hydroxylation activity in relation to the activity of NADPH-linked electron transport system has not yet been reported.…”

mentioning

confidence: 99%

Effect of Vitamin C Deficiency on the Metabolism of Drugs and Nadph-Linked Electron Transport System in Liver Microsomes

Kato

Takanaka

Oshima

1969

Japanese Journal of Pharmacology

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mentioning

confidence: 99%

Effect of Vitamin C Deficiency on the Metabolism of Drugs and Nadph-Linked Electron Transport System in Liver Microsomes

Kato

Takanaka

Oshima

1969

Japanese Journal of Pharmacology

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“…Monodehydroascorbate radical is believed to be an intermediate in microsomal electron transport, oxidation, and hydroxylation reactions (128,222,304). Moderate concentrations of atmospheric ozone increase oxygen consumption of mitochondria (219,220), suggesting that oxidation of the sulfur atom of homocysteine thiolactone within thioretinaco by ozone may produce sulfonium atoms as the active site of oxidative phosphorylation.…”

Section: Thioretinamide Thioretinaco Carcinogenesis and Atherogenesismentioning

confidence: 98%

Homocysteine Metabolism, Atherosclerosis, and Diseases of Aging

McCully

2015

Comprehensive Physiology

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The importance of homocysteine in vascular function and arteriosclerosis was discovered by demonstration of arteriosclerotic plaques in children with homocystinuria caused by inherited enzymatic deficiencies of cystathionine synthase, methionine synthase, or methylene-tetrahydrofolate reductase. According to the homocysteine theory of arteriosclerosis, an elevated blood homocysteine level is an important risk factor for atherosclerosis in subjects without these rare enzymatic abnormalities. The homocysteine theory is supported by demonstration of arterial plaques in experimental animals with hyperhomocysteinemia, by discovery of a pathway for conversion of homocysteine thiolactone to sulfate in cell cultures from children with homocystinuria, and by demonstration of growth promotion by homocysteic acid in normal and hypophysectomized animals. Studies with cultured malignant cells revealed abnormal homocysteine thiolactone metabolism, resulting in homocysteinylation of proteins, nucleic acids, and glycosaminoglycans, explaining the abnormal oxidative metabolism, abnormalities of cellular membranes, and altered genetic expression observed in malignancy. Abnormal homocysteine metabolism in malignant cells is attributed to deficiency of thioretinamide, the amide synthesized from retinoic acid and homocysteine thiolactone. Two molecules of thioretinamide combine with cobalamin to form thioretinaco. Based on the molecular structure of thioretinaco, a theory of oxidative phosphorylation was proposed, involving oxidation to a disulfonium derivative by ozone, and binding of oxygen, nicotinamide adenine dinucleotide and phosphate as the active site of adenosine triphosphate synthesis in mitochondria. Obstruction of vasa vasorum by aggregates of microorganisms with homocysteinylated low-density lipoproteins is proposed to cause ischemia of arterial wall and a microabscess of the intima, the vulnerable atherosclerotic plaque.

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“…Suggested ascorbic acid (AA) functions include being a direct chemical co-factor (1 3); a reducing agent in collagen hydroxylation reactions (1 4-1 5); an antioxidant in concert with glutathione and superoxide dismutase (16)(17)(18)(19)(20)(21); a link in electron transfer reactions (22); a radiation absorber (23); and a redox coupler involved in mediating the hexose monophosphate shunt (24,25). In this study we explore factors affecting unilateral and "net" ascorbic movement across the RPE mounted as a sheet in an Ussing chamber.…”

Section: Introductionmentioning

confidence: 99%

Active transport of ascorbic acid across the retinal pigment epithelium of the bullfrog

DiMattio

Streitman

1991

Current Eye Research

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Known functions of the RPE include glucose, water and retinoid transports; an ion transport mechanism utilizing a Na(+)-K(+)-ATPase pump located in the apical membrane has been proposed. Recent studies with cultured RPE cells of cat and bovine indicate that the RPE takes up ascorbate by an active mechanism. In this study we use a mounted bullfrog RPE preparation to study unidirectional and net fluxes of radiolabeled (14C)-ascorbic acid (AA), (14C)-dehydroascorbic acid, (3H)-L-glucose(L-glu) and (14C)-3-O-methyl-D-glucose(mD-glu) in an effort to explore the mechanism whereby AA moves across this tissue. Comparative flux studies with AA indicated that the retina to blood side (apical to basal:AB) flux of AA was more than 6x that of L-glu, a passive marker of comparable size. The reverse BA flux of AA was not significantly different from that of L-glu. Flux studies of L-glu, mD-glu and dehydroascorbic acid revealed no "net" flux across the mounted RPE; significantly, only AA demonstrated a net flux from retina to choroid (AB). The AB flux of reduced ascorbate was significantly greater than that of dehydroascorbic acid indicating specificity of carrier mediation. Apical ouabain (10(-4) M) and sodium replacement in the bathing medium reduced the AB and net flux of AA significantly suggesting the requirement of a functioning Na(+)-K(+)-ATPase on the apical side membrane of the RPE. Energy blocker, dinitrophenol decreased unidirectional AB and net AA fluxes.(ABSTRACT TRUNCATED AT 250 WORDS)

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Role of Ascorbic Acid in Microsomal Electron Transport and the Possible Relationship to Hydroxylation Reactions

Cited by 72 publications

References 20 publications

Effect of Vitamin C Deficiency on the Metabolism of Drugs and Nadph-Linked Electron Transport System in Liver Microsomes

Effect of Vitamin C Deficiency on the Metabolism of Drugs and Nadph-Linked Electron Transport System in Liver Microsomes

Homocysteine Metabolism, Atherosclerosis, and Diseases of Aging

Active transport of ascorbic acid across the retinal pigment epithelium of the bullfrog

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