Tissue Levels and Optimum Dosage of Vitamin C in Guinea Pigs

Ginter, E; Bobek, P; Vargová, D.

doi:10.1159/000176259

Cited by 28 publications

(8 citation statements)

References 21 publications

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“…(' Table 3; Ginter et al, 1979). Further, a recent report on the effects of ascorbate deficiency on the in vivo synthesis of carnitine in guinea pigs supports the contention that SDR is important for maintenance of ascorbate levels.…”

Section: Discussionmentioning

confidence: 75%

Tissue, Subcellular, and Submitochondrial Distributions of Semidehydroascorbate Reductase: Possible Role of Semidehydroascorbate Reductase in Cofactor Regeneration

Diliberto

Dean

Carter

et al. 1982

Journal of Neurochemistry

102

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The immediate product of ascorbate oxidation coupled to dopamine-beta-hydroxylation is not dehydroascorbate, as previously thought, but rather semidehydroascorbate. For this reason, the possible participation of the enzyme semidehydroascorbate reductase (SDR) in cofactor regeneration was investigated. In the adrenal medulla, the primary subcellular localization of this reductase was shown to be in the mitochondria. Submitochondrial fractionation studies indicated that SDR is an outer membrane protein. Thus, although dopamine-beta-hydroxylase and SDR have different subcellular localizations, a physiological role for SDR in beta-hydroxylation still appears plausible through reduction of cytosolic semidehydroascorbate. The specific activities of SDR in various rat and guinea pig tissues appear to parallel their ascorbate contents, suggesting a similar participation of SDR in ascorbate metabolism in other tissues.

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Section: Discussionmentioning

confidence: 75%

Tissue, Subcellular, and Submitochondrial Distributions of Semidehydroascorbate Reductase: Possible Role of Semidehydroascorbate Reductase in Cofactor Regeneration

Diliberto

Dean

Carter

et al. 1982

Journal of Neurochemistry

102

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“…It has also been reported, but not in fish, that megadoses of ascorbic acid have adverse effects on growth and food consumption (Ginter, Bobek & Vargova 1979;Keith, Libke & Driskell 1981). In the present study tilapias fed diets containing megadoses of ascorbic acid (300 and 400mg/100g of diet) exhibited growth retardation in comparison with those fed the diet containing 125mg ascorbic acid/lOOg.…”

Section: Discussionmentioning

confidence: 99%

“…Later workers (Nandi et al 1973;Keith & Pelletier 1974), using a single daily dose of ascorbic acid, found no increase in tissue ascorbate concentration when the dose exceeded the requirement. Ginter et al (1979) showed that when ascorbic acid was administered more frequently to guinea pigs, either in the diet or in drinking water, that tissue ascorbate concentrations were more closely correlated with the level of intake. In the present study, ascorbic acid was administered in the feed four times daily and tissue ascorbate concentrations continued to increase with increasing dietary ascorbic acid up to the maximum evaluated (400mg/100g) with a high correlation between tissue level and dose.…”

Section: Discussionmentioning

confidence: 99%

Water-soluble vitamin requirements of tilapia: ascorbic acid (vitamin C) requirement of Nile tilapia, Oreochromis niloticus (L.)

1994

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The quantitative dietary ascorbic acid requirements of fingerling Nile tilapia, Oreochromis niloticus L., were assessed by feeding seven diets containing graded supplements of this vitamin (0,50,75,100,125,300 and 400mg/100g dry diet) to triplicate groups of fish for 12 weeks. Fish fed the diet devoid of ascorbic acid exhibited significantly (P < 0-01) poorer growth and higher condition factor. Food conversion and protein efficiency ratios were improved with increasing dietary ascorbic acid level up to 125mg/100g of dry diet. Protein utilization, haematocrit, haemoglobin level and tissue ascorbate concentrations were depressed in fish fed the ascorbic-acid-free diet. Tissue ascorbate concentrations, especially for liver, were highly correlated with dietary ascorbic acid level. Fish fed the ascorbic-acid-free diet exhibited deficiency signs including erratic and convulsive swimming, anorexia, lethargy, caudal fin erosion, skin haemorrhages and mortality. Based on the nutritional and pathological parameters investigated, the recommended dietary inclusion level is 125mg/100g dry diet, which is equivalent to a net requirement (after processing and storage) of 42mg/100g diet.

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“…Higher concentrations resulted in a rapid decline in lipid peroxidation in the adrenal and a more gradual decline in testicular lipid peroxidation, probably as a result of the antioxidant properties of ascorbate being manifested. The normal level of ascorbate in the guinea pig adrenal is nearly 1 x 1O-2M, a concentration at which ascorbate may exert primarily antioxidant effects (15,16). However, upon stimulation by ACTH, the ascorbate concentration of the adrenal cortex decreases to levels which may promote lipid peroxidation (17).…”

Section: Discussionmentioning

confidence: 99%

Lipid Peroxidation in Adrenal and Testicular Microsomes

Brogan¹,

Miles²,

Colby³

1981

Environmental Health Perspectives

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Studies were carried out to determine the actions of and interactions between ascorbate, NADPH, Fe2 +, and Fe3 + on lipid peroxidation in adrenal and testicular microsomes. Ascorbateinduced malonaldehyde production was maximal in adrenal and testicular microsomes at an ascorbate concentration of 1 x 10M. Fe2 +, at levels between 10 and 10-3M, produced concentration-dependent increases in lipid peroxidation in adrenal and testicular microsomes; Fe2 + had a far greater effect than Fe3 + in both tissues. In liver microsomes, by contrast, Fe2 + and Fe3`had quantitatively similar effects on lipid peroxidation. NADPH alone had no effect on malonaldehyde production in adrenal or testicular microsomes. However, in the presence of low Fe2+ concentrations (106M), NADPH stimulated adrenal malonaldehyde production. The stimulation of lipid peroxidation by NADPH plus low Fe2 + was not demonstrable in testicular microsomes nor in adrenal microsomes which had been heat-treated to inactivate microsomal enzymes. Testicular malonaldehyde production was stimulated by NADPH if Fe3 + (5 x 10-5 to 1 x 103M) was added to the incubation medium; the stimulation was not demonstrable in heat-treated microsomes. Fe3 +plus NADPH had little effect on adrenal lipid peroxidation. In the presence of high Fe2+ levels (10-3M), NADPH produced a concentration-dependent inhibition of adrenal lipid peroxidation; the inhibition was fully demonstrable in heat-treated microsomes. NADPH similarly inhibited ascorbate-induced lipid peroxidation in adrenal microsomes. In testicular microsomes, NADPH did not inhibit ascorbate or Fe2 + -induced lipid peroxidation. The results indicate that various endogenous substances may be important in the control of adrenal and testicular lipid peroxidation and that the nature of the regulation differs from tissue to tissue.

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Tissue Levels and Optimum Dosage of Vitamin C in Guinea Pigs

Cited by 28 publications

References 21 publications

Tissue, Subcellular, and Submitochondrial Distributions of Semidehydroascorbate Reductase: Possible Role of Semidehydroascorbate Reductase in Cofactor Regeneration

Tissue, Subcellular, and Submitochondrial Distributions of Semidehydroascorbate Reductase: Possible Role of Semidehydroascorbate Reductase in Cofactor Regeneration

Water-soluble vitamin requirements of tilapia: ascorbic acid (vitamin C) requirement of Nile tilapia, Oreochromis niloticus (L.)

Lipid Peroxidation in Adrenal and Testicular Microsomes

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