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PubMedDate not supplied

Biological function of ascorbic acid and the pathogenesis of scurvy: a working hypothesis.

This communication advances the proposal that all the diverse manifestations of scurvy can be attributed to depolymerisation of ground substance glycosaminoglycans brought about by exposure to uninhibited cellular hyaluronidase. It suggests that ascorbic acid exerts its prime biological function indirectly by incorporation into a glycosaminoglycan residue to form the physiological hyaluronidase inhibitor. The therapeutic implications of this working hypothesis are briefly discussed.

Ascorbic Acid↗
PubMedDate not supplied

Ascorbate blocks amphetamine-induced turning behavior in rats with unilateral nigro-striatal lesions.

Unilateral nigro-striatal lesions were produced in rats using 6-hydroxydopamine. Intraperitoneal injections of amphetamine induced circling behavior in these rats due to release of striatal dopamine contralateral to the lesion. Intraperitoneal injections of 1 g/kg of ascorbic acid elevated brain ascorbate. Ascorbate, like other drugs blocking dopamine receptors, attenuated the amphetamine-induced turning behavior. Thus, ascorbic acid might have a role in regulating dopaminergic transmission and could be of therapeutic value in disorders involving functional dopamine excess.

Animals↗
PubMed1988

A protocol for the successful long-term enzyme replacement therapy of scurvy in guinea pigs.

Gulonolactone oxidase, a key enzyme in the biosynthesis of ascorbic acid, is missing from guinea pigs and certain other scurvy-prone species. Weekly intraperitoneal injections of glutaraldehyde cross-linked immunoprecipitates of this enzyme have been shown to provide guinea pigs with the capability of synthesizing their own ascorbic acid and of surviving without an exogenous source of this vitamin. This protocol, however, was successful in only a small percentage of the animals tested. The reasons for the limited therapeutic success were investigated. Apparently, the gulonolactone oxidase-treated guinea pigs fed without ascorbic acid were receiving insufficient nutrition. By supplementing these enzyme-treated animals with vitamins A, B, D and E and selenium, we successfully maintained a high proportion of guinea pigs fed without vitamin C.

Animals↗
PubMed1993

Chemo-immunotherapeutical studies on Dalton's lymphoma in mice using cisplatin and ascorbic acid: synergistic antitumor effect in vivo and in vitro.

Combined effects of ascorbic acid (vitamin C) and cisplatin on the growth of Dalton's lymphoma in C3H/He mice was investigated. Chemotherapy with sub-therapeutical dose (3 mg/kg) enabled to increase the survival time of the tumor bearing mice without any tumor free survivors. Ascorbic acid enhances the antitumor effect of cisplatin in vivo resulting in 60/70 day survivors along with tumor free survivors. Ascorbic acid also enhances the efficacy of low dose of cisplatin (5 micrograms/ml) in vitro. Tumor cells incubated with cisplatin and ascorbic acid, when injected into normal mice, exhibited inhibited growth resulting in an increased life span of tumor bearing mice and tumor free survivors. Inoculation of tumor cells incubated with cisplatin (5 micrograms/ml) and different concentrations (25 or 50 micrograms/ml) of ascorbic acid resulted in 30% tumor free mice which was not observed when concentration of cisplatin increased to 10 micrograms/ml in the medium. A possible cause of the enhancement of cisplatin-induced tumor growth inhibition may be the modulation of permeability of tumor cell membrane by ascorbic acid which increases the uptake of cisplatin into tumor cells, making less efficient the DNA repair machinery due to increased efficiency of adduct formation in DNA molecule. Possibly, this effect of ascorbic acid renders cisplatin more effective as an antitumor agent.

Animals↗
PubMed2004

Alpha-hydroxyacids and carboxylic acids.

The carboxylic acids include alpha-hydroxyacids (AHAs), polyhydroxy acids (PHAs), aldobionic acids (ABAs), retinoic acid, vitamin C and azelaic acid. They all have therapeutic actions. AHAs, PHAs and ABAs are organic hydroxyacids, a group of natural and physiological substances which can modulate skin keratinization and increase biosynthesis of dermal components. Because of these effects, AHAs, PHAs and ABAs are therapeutically effective or beneficial for topical treatment of dry skin, rough skin, acne, rosacea, warts, eczema, psoriasis and skin changes associated with ageing, including wrinkles and photoageing. In addition, PHAs and ABAs, which are antioxidants, are topically beneficial for sensitive or diseased skin and for the prevention of oxidative damage caused by UV radiation. The vitamin A derivatives, known as retinoids, include three that are found physiologically. Retinoic acid is the most potent of these in promoting proliferation and differentiation of epithelial cells, and in stimulating biosynthesis of collagen I and III. Because of these actions, retinoic acid is therapeutically effective for topical treatment of acne, actinic keratoses and photoaged skin. Vitamin C, which is l-ascorbic acid and a lactone form of 3-keto-polyhydroxy acid, is a water-soluble antioxidant. Because of this property vitamin C has been promoted for topical prevention of skin damage caused by UV radiation. Azelaic acid has been shown to normalize keratinization in the follicular infundibulum, exert an antibacterial effect against Propionibacterium acnes and inhibit melanogenesis and so has been used for topical treatment of acne and melasma. The carboxylic acids display similarities and differences in their topical actions and therapeutic applications.

Journal Article↗
PubMedDate not supplied

Stabilization of (90)y-labeled DOTA-biomolecule conjugates using gentisic acid and ascorbic acid.

Radiolytic degradation of radiolabeled compounds is a major challenge for the development of new therapeutic radiopharmaceuticals. The goal of this study is to explore the factors influencing the solution stability of a (90)Y-labeled DOTA-peptide conjugate (RP697), including the amount of total activity, the activity concentration, the stabilizer concentration, and the storage temperature. In general, the rate of radiolytic decomposition of RP697 is much slower at the lower activity concentration (<4 mCi/mL) than that at the higher concentration (>10 mCi/mL). RP697 remains relatively stable at the 20 mCi level and room temperature while it decomposes rapidly at the 100 mCi level under the same storage conditions. Radical scavengers, such as gentisic acid (GA) and ascorbic acid (AA), were used in combination with the low temperature (-78 degrees C) to prevent the radiolytic decomposition of RP697. It was found that RP697 remains stable for at least 2 half-lives of (90)Y when GA or AA (10 mg for 20 mCi of (90)Y) is used as a stabilizer when the radiopharmaceutical composition is stored at -78 degrees C. The stabilizer (GA and AA) can be added into the formulation either before or after radiolabeling. The post-labeling approach is particularly useful when the use of a large amount of the stabilizer interferes with the radiolabeling. The radiopharmaceutical composition developed in this study can also apply to other (90)Y-labeled DOTA-biomolecule conjugates. The amount of the stabilizer used in the radiopharmaceutical composition and storage temperature should be adjusted according to the sensitivity of the radiolabeled DOTA-biomolecule conjugate toward radiolytic decomposition.

Ascorbic Acid↗
PubMed2000

Effect of aspirin on blood-lipid interaction and lipid peroxidation phenomena in relation to partition coefficient and biological activity.

Considering the lipophilicity of aspirin (log P = -1.15), a significant contributor to its action mechanism, interaction of the drug with the whole lipids of goat blood have been investigated using phospholipid binding and lipid peroxidation phenomena as the parameters under investigation. The lipid content change along with the peroxidation induced by aspirin and its suppression with ascorbic acid had been quantitatively measured. Significant loss in phospholipid was observed after incubation of whole blood with aspirin in varying periods of time. This may be ascribed to binding affinity of aspirin with lipid constituents in blood, which may have potential role in its therapeutic effect. Lipid peroxidation induction potential of aspirin caused significant extent of peroxidation. Ascorbic acid, an antioxidant could significantly reduce aspirin induced lipid peroxidation.

Animals↗
PubMed1980

The therapeutics of peptic ulcers: clinical evaluation of C-Fe therapy.

Ascorbic acid and ferrous sulfate were given to peptic ulcer patients (C-Fe therapy). In gastric ulcer patients, the healing index of the C-Fe therapy group was significantly higher than that of controls, but in duodenal ulcer patients, no significant difference was observed between the healing index of the C-Fe therapy group and that of controls. According to these results, it was concluded that C-Fe therapy was effective in healing gastric ulcers and that the cause of duodenal ulcers might depend more on aggressive factors than that of gastric ulcers.

Adult↗
PubMed2006

In vivo and in vitro antitumor effect of ascorbic acid, lysine, proline, arginine, and green tea extract on human fibrosarcoma cells HT-1080.

Current treatment of fibrosarcoma, an aggressive cancer of the connective tissue, is generally associated with poor prognosis. Matrix metalloproteinases (MMPs), vascular endothelial growth factor (VEGF), and constituents of the extracellular matrix (ECM), such as fibronectin, play a critical role in angiogenesis and underlie neoplastic invasion and metastasis. This and anticancer properties of lysine, proline, arginine, ascorbic acid, and green tea extract (NM) prompted us to investigate the effect of these nutrients in vitro on human fibrosarcoma cells HT-1080 by measuring cell proliferation, modulation of MMP-2 and MMP-9, and invasive potential. In vivo, we studied the growth of human fibrosarcoma HT-1080 cells in athymic nude mice and the expression of MMPs and VEGF. Cell proliferation was evaluated by MTT assay, MMP expression by gelatinase zymography, and invasion through Matrigel and migration by scratch assay. Tumors were excised, weighed, and processed for histology in both the control and nutrient-supplemented groups. Results showed NM inhibited the growth and reduced the size of tumors in nude mice; decreased MMP-9 and VEGF secretion was found in the supplemented group tissues. NM inhibited invasion through Matrigel and migration with total inhibition at 1,000 microg/mL. These results offer promise in the therapeutic use of the nutrient mixture of lysine, proline, arginine, ascorbic acid, and green tea extract tested in the treatment of fibrosarcoma.

Animals↗
PubMedDate not supplied

Paraquat suicide in a young woman: results of therapy directed against the superoxide radical.

The clinical course of a young woman following two separate suicide attempts using the herbicide paraquat is reported. The patient survived an intramuscular injection of paraquat almost asymptomatically, but later exhibited a typical fatal course with fulminant proliferative pulmonary fibrosis after an intravenous injection. Fibrosis and death occurred despite a therapeutic regimen based upon a known action of paraquat, the generation of superoxide (O(2)[unk]), using superoxide dismutase, α-tocopherol, and ascorbic acid in conjunction with forced diuresis and prednisone. While treatment failed explanations for the failure of therapy in this case and current therapeutic alternatives are discussed so that they may be considered when future cases are encountered.

Adult↗
PubMed2003

Pulmonary bioavailability of ascorbic acid in an ascorbate-synthesising species, the horse.

Vitamin C (ascorbic acid) is a non-enzymatic antioxidant important in protecting the lung against oxidative damage and is decreased in lung lining fluid of horses with airway inflammation. To examine possible therapeutic regimens in a species with ascorbate-synthesising capacity, we studied the effects of oral supplementation of two forms of ascorbic acid, (each equivalent to 20 mg ascorbic acid per kg body weight) on the pulmonary and systemic antioxidant status of six healthy ponies in a 3 x 3 Latin square design. Two weeks supplementation with ascorbyl palmitate significantly increased mean plasma ascorbic acid concentrations compared to control (29 +/- 5 and 18 +/- 7 micromol/l, respectively; p < 0.05). Calcium ascorbyl-2-monophosphate, a more stable form of ascorbic acid, also increased mean plasma ascorbic acid concentrations, but not significantly (23 +/- 1 micromol/l; p = 0.07). The concentration of ascorbic acid in bronchoalveolar lavage fluid increased in five out of six ponies following supplementation with either ascorbyl palmitate or calcium ascorbyl-2-monophosphate compared with control (30 +/- 10, 25 +/- 4 and 18 +/- 8 micromol/l, respectively; p < 0.01). Neither supplement altered the concentration of glutathione, uric acid or alpha-tocopherol in plasma or bronchoalveolar lavage fluid. In conclusion, the concentration of lung lining fluid ascorbic acid is increased following ascorbic acid supplementation (20 mg/kg body weight) in an ascorbate-synthesising species.

Animals↗
PubMed2006

Myelin disorders: Causes and perspectives of Charcot-Marie-Tooth neuropathy.

Charcot-Marie-Tooth (CMT) disease is a common hereditary neuropathy that causes progressive distally pronounced muscle weakness and can lead to life-long disability in patients. In most cases, the disorder has been associated with a partial duplication of human chromosome 17 (CMT1A), causing 1.5-fold overexpression of the peripheral myelin protein 22 kDa (PMP22). Increased PMP22 gene dosage results in demyelination, secondary axonal loss, and neurogenic muscle atrophy. Experimental therapeutic approaches based on the role of progesterone and ascorbic acid in myelin formation recently have reached preclinical proof-of-principle trials in rodents. It was shown that progesterone receptor antagonists can reduce PMP22 overexpression and clinical severity in a CMT1A rat model. Furthermore, ascorbic acid treatment reduced premature death and demyelination in a CMT1A mouse model. Thus, basic research has opened up new vistas for the understanding and treatment of hereditary neuropathies.

Animals↗