Ascorbic Acid Effects on Vitamin D Hormone Metabolism and Binding in Guinea Pigs

Сергеев, И. Н.; Arkhapchev, Yriy P.; Спиричев, В. Б.

doi:10.1093/jn/120.10.1185

Cited by 38 publications

(16 citation statements)

References 21 publications

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“…GSH ester slowed the disappearance of osteoid material characteristically seen in scurvy. In addition to the well-studied effect of scurvy on hydroxylation reactions involved in collagen synthesis, recent work suggests that ascorbate-dependent hydroxylation may also be closely connected with vitamin D metabolism and formation of bone (29).…”

Section: Discussionmentioning

confidence: 99%

Glutathione ester delays the onset of scurvy in ascorbate-deficient guinea pigs.

Mårtensson

Han

Griffith

et al. 1993

Proc. Natl. Acad. Sci. U.S.A.

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Previous studies showed that administration of ascorbate to glutathione (GSH)-deflcient newborn rats and guinea pigs prevented toxicity and mortality and led to increased tissue and mitochondrial GSH levels; ascorbate thus spares GSH. In recent work it was shown that glutathione (GSH) deficiency in newborn rats (1-4, 30) and in guinea pigs (5), produced by administration of buthionine sulfoximine [a transition-state inhibitor of y-glutamylcysteine synthetase (6-8)], leads to death within a few days. In newborn rats (which apparently do not synthesize ascorbate), GSH deficiency is associated with severe mitochondrial and other cell damage (30) in kidney (1, 2), lung (1, 2), liver (1, 2), brain (1-3), and lens (1, 2, 4, 9). Similar results were found in guinea pigs (10). GSH deficiency in newborn rats (2) leads to decreased tissue ascorbate levels and to increased dehydroascorbate levels. GSH deficiency in adult mice does not lead to early mortality but is associated with damage to skeletal muscle (11, 12), lung (12, 13), jejunal epithelium (14), and colon epithelium (14). The relatively decreased morbidity that accompanies GSH deficiency in adult mice may be ascribed, at least in part, to their ability to synthesize ascorbate (1). Mortality due to GSH deficiency in newborn rats (1, 2, 4) and in guinea pigs (10), as well as tissue damage in these animals and in adult mice, may be decreased or prevented by administration of GSH esters or of ascorbate (1-4, 30). Newborn rats develop cataracts when subjected to mild GSH deficiency (2, 4), and cataracts are prevented by giving GSH esters or ascorbate; interestingly, dehydroascorbate protects in this model because of the availability of moderate GSH levels (2). These experiments indicate that (i) ascorbate spares GSH, (ii) GSH and ascorbate have actions in common in the destruction of reactive oxygen species, and (iii) reduction of dehydroascorbate to ascorbate is a significant physiological function of GSH (2). Because ascorbate can serve as an essential antioxidant in GSH deficiency, it is of interest to ask the converse question-i.e., can GSH function in place of ascorbate? In the present studies we used the ascorbate-deficient guinea pig model. Because administered GSH is not significantly transported into most cells, we gave GSH monoethyl ester, which is efficiently transported and split to form GSH intracellularly (15)(16)(17).A preliminary account of these studies has appeared (18). EXPERIMENTAL PROCEDURESMaterials. Male Hartley guinea pigs (260-300 g) were obtained from Hilltop Labs (Scottsdale, PA). The control diet was standard guinea pig chow from Purina; the ascorbatedeficient diet was from United States Biochemical. All animals had free access to water. GSH was obtained from Sigma. GSH monoethyl ester was prepared as the hydrosulfate salt (17,19,20,31).Methods. Control guinea pigs were given chow ad libitum; ascorbate-deficient animals were maintained on an ascorbate-deficient diet for 9 or 21 days. Control animals received no treatment; animals on...

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Section: Discussionmentioning

confidence: 99%

Glutathione ester delays the onset of scurvy in ascorbate-deficient guinea pigs.

Mårtensson

Han

Griffith

et al. 1993

Proc. Natl. Acad. Sci. U.S.A.

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“…Vitamin D status should be carefully defined as sufficient, insufficient, or deficient based on mechanistic studies and direct and indirect evidence-based approach. The US Institute of Medicine (IOM) [22,23], the Endocrine Society [24], the European Food Safety Authority [25], and health regulatory agencies of other European countries [26,27] [1,26,29,30]. Extra-renal production of 1,25(OH) 2 D 3 and its possible significance for paracrine/autocrine regulation of cellular functions is plausible [1,3], but this production does not appear to contribute to maintaining circulating 1,25(OH) 2 It is also worth mentioning that rickets and osteomalacia are observed when 25(OH)D is "undetectable" in blood (usually, it means below 0.5-5 ng/mL depending on the assay) and that the optimal bone growth and remodeling as well as maximum intestinal Ca 2+ absorption [the major physiological functions of 1,25(OH) 2 D 3 ] can be maintained in healthy individuals at 25(OH)D concentrations in the range of 10-20 ng/mL [probably, the lower limit is sufficient because it will not limit the 1,25(OH) 2 D 3 production].…”

Section: Introductionmentioning

confidence: 99%

Vitamin D-mediated apoptosis in cancer and obesity

Сергеев

2014

Hormone Molecular Biology and Clinical Investigation

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Low vitamin D status has been associated with increased risk of several cancers and obesity; concurrently, obesity and cancer have been linked to impaired vitamin D status. In both cancer and obesity, selective elimination of cancer cells and adipocytes can result in decreasing tumor size and a long-term reduction in adipose tissue mass. These effects can be achieved through induction of apoptotic cell death. -dependent apoptotic proteases as promising targets for discovery of new therapeutic and preventive agents for cancer and obesity. The concept of maintaining an increased vitamin D status for protecting against cancer and decreasing adiposity also warrants further evaluation.

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“…However, supplementation of the diet of two strains of 71-week-old hens (LB Brown and LSL White) with 2 mg/kg calcitriol for 8 weeks lowered the rate of damaged eggs and concurrent use of 100 mg/ kg ascorbic acid further decreased shell breakage (Weiser et al, 1992). The dramatic response to ascorbic acid was ascribed to its synergistic role in the hydroxylation of cholecalciferol (Weiser et al, 1988), similar to the response observed in guinea pigs (Sergeev et al, 1990) and the terminal differentiation of cultured chondrocytes through promotion of calcitriol synthesis (Farquharson et al, 1998). Based on the response of old hens to ascorbic acid (Weiser et al, 1992) it was postulated that weak shells towards the end of the production cycle may be the result of decreased biosynthesis of ascorbic acid, decreased tissue ascorbic acid, and the downstream consequences on synthesis of calcitriol.…”

Section: Introductionmentioning

confidence: 54%

Ascorbic acid biosynthesis in hens producing strong and weak eggshells

Maurice

Lightsey²,

Toler

2004

Br. Poultry Sc.

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1. An experiment was conducted with two strains of layers to ascertain whether the reduction in eggshell strength occurring at the end of the production cycle is the result of reduced ascorbic acid biosynthesis. 2. Hens producing strong and weak eggshells were identified within each strain and egg production, egg weight, per cent shell, shell surface density, plasma, adrenal and hepatic ascorbic acid and renal L-gulonolactone oxidase activity were measured. 3. The strains differed in ascorbic acid synthesis, as measured by L-gulonolactone oxidase activity, and tissue ascorbic acid concentration. 4. Comparison of results from birds producing eggs of similar weight but markedly different in shell strength detected neither a shell strength group x strain interaction nor an effect of shell strength group on plasma and hepatic ascorbic acid and activity of L-gulonolactone oxidase. 5. The results did not support the hypothesis that tissue ascorbate and ascorbic acid biosynthesis are reduced in old hens producing weak eggshells.

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Ascorbic Acid Effects on Vitamin D Hormone Metabolism and Binding in Guinea Pigs

Cited by 38 publications

References 21 publications

Glutathione ester delays the onset of scurvy in ascorbate-deficient guinea pigs.

Glutathione ester delays the onset of scurvy in ascorbate-deficient guinea pigs.

Vitamin D-mediated apoptosis in cancer and obesity

Ascorbic acid biosynthesis in hens producing strong and weak eggshells

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