Release Of Ascorbic Acid Research Articles

Investigation of neoascorbigen

The synthesis of N-methoxyascorbigen (neoascorbigen) — a natural substance from plants of the Cruciferae family — and also N-ethoxyascorbigen is described. In an acidic media under drastic conditions N-alkoxyascorbigens undergo transformations with the release of ascorbic acid and the formation of oligomers of 1-alkoxy-3-methyleneindolenine or with opening of the lactone ring, decarboxylation, and dehydration and the formation of 2-hydroxy-3-(1-alkoxy-3-indolyl)-4-hydroxymethylcyclopent-2-enone. Amides of neoascorbigen, 3-O-methylglycoside of N-ethoxyascorbigen, and the product of the reduction of N-ethoxyascorbigen by sodium borohydride were obtained for the first time.

On the mechanism of d-amphetamine-induced changes in glutamate, ascorbic acid and uric acid release in the striatum of freely moving rats.

1. The effects of systemic, intrastriatal or intranigral administration of d-amphetamine on glutamate, aspartate, ascorbic acid (AA), uric acid, dopamine (DA), dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA) and 5-hydroxyindoleacetic acid (5-HIAA) concentrations in dialysates from the striatum of freely-moving rats were evaluated using microdialysis. 2. d-Amphetamine (2 mg kg-1) given subcutaneously (s.c.) increased DA, AA and uric acid and decreased DOPAC + HVA, glutamate and aspartate dialysate concentrations over a 3 h period after d-amphetamine. 5-HIAA concentrations were unaffected. Individual changes in glutamate and AA dialysate concentrations were negatively correlated. 3. d-Amphetamine (0.2 mM), given intrastriatally, increased DA and decreased DOPAC + HVA and aspartate dialysate concentrations, but failed to change those of glutamate, AA uric acid or 5-HIAA, over a 2 h period after d-amphetamine. Haloperidol (0.1 mM), given intrastriatally, increased aspartate concentrations without affecting those of glutamate or AA. 4. d-Amphetamine (0.2 mM), given intranigrally, increased AA and uric acid dialysate concentrations and decreased those of glutamate, aspartate and DA; DOPAC + HVA and 5-HIAA concentrations were unaffected. 5. These results suggest that d-amphetamine-induced increases in AA and uric acid and decreases in glutamate concentrations are triggered at nigral sites. The changes in aspartate levels may be evoked by at least two mechanisms: striatal (mediated by inhibitory dopaminergic receptors) and nigral (activation of amino acid carrier-mediated uptake).

Chronic effects of an aminosteroid on microdialytically measured parameters after experimental middle cerebral artery occlusion in the rat

The effects of the neuroprotective aminosteroid U74006F (tirilazad mesylate, Freedox) were monitored microdialytically in rat cortex during three 4 h periods beginning immediately, 25 h and 49 h after permanent middle cerebral artery occlusion. Either U74006F or vehicle only was administered 15 min, 2 h, 6 h, 12 h and 24 h after operation. The dialysate was analysed for on-line pH, ascorbic acid, uric acid, glucose and lactate. The efficacy of post-ischaemic treatment was shown by: a) lesion volume 53h after operation was significantly smaller in U74006F-treated animals; b) microdialytic findings were very similar to those found previously with pre-ischaemic drug application (reduction in release of ascorbic acid, uric acid and lactate, increased pH); c) an effect of U74006F on lactate release could still be seen on days 2 and 3; and d) increases in uric acid on days 2 and 3, possibly reflecting delayed cell death, were smaller in aminosteroid treated animals.

Involvement of the corticostriatal glutamatergic pathway in ethanol‐induced ascorbic acid release in rat striatum

The mechanism of ethanol-induced ascorbic acid (AA) release in striatum is not well understood. In the present work, the possible involvement of NMDA receptors in the corticostriatal pathway was studied by microdialysis coupled to high performance liquid chromatography with electrochemical detection. Ethanol (3.0 g/kg i.p.) stimulated significant striatal AA release to more than 200% above the baseline. This effect of ethanol could be partially antagonized by amantadine, a non-selective NMDA receptor antagonist and dopamine releaser, at a dose of 200 mg/kg i.p. and significantly antagonized by MK-801, a non-competitive NMDA receptor antagonist, at the doses of 0.5 and 1.0 mg/kg i.p. Furthermore, deafferentation of the glutamatergic projection from cortex to striatum by undercutting the prefrontal cortex completely eliminated ethanol-induced AA release in rat striatum. The basal level of AA in striatum could only be reduced by high doses of MK-801, but not by low doses of MK-801, amantadine or decortication. The results further confirm that NMDA receptors are involved in ethanol-induced AA release and provide the first evidence for the necessity of the activation of corticostriatal glutamatergic pathway in ethanol-induced AA release in rat striatum.

Acute effects of an aminosteroid on microdialytically measured parameters after experimental middle cerebral artery occlusion in the rat

The effects of the neuroprotective aminosteroid U74389G were monitored microdialytically in rat cortex during 4 h after permanent middle cerebral artery occlusion. Either U74389G or vehicle only was administered one hour before and 2 h after operation. The dialysate was analysed for on-line pH, ascorbic acid, uric acid, glucose and lactate. In aminosteroid treated animals the levels of ascorbic and uric,acids were lower in dialysates after occlusion, total release of lactate was significantly reduced and online pH was significantly higher than in control animals. Lesion volume at 4 h, which was significantly reduced in treated animals correlated positively with ascorbic acid release and on-line pH. Results suggest that neuroprotective effects of aminosteroids might be explained by: (a) preservation of intracellular levels of the radical scavenger ascorbic acid with possible concomitant reduction of glutamate release; and (b) reduced lactate release and increased pH which might influence oedema positively.

Dl-Fenfluramine inhibits ethanol-induced ascorbic acid release in rat striatum studied by microdialysis.

The effects of dl -fenfluramine, dl -5-hydroxytryptophan(5-HTP) and fluoxetine on ethanol-induced striatal ascorbic acid (AA) release in rat were studied by microdialysis coupled to high performance liquid chromatography with electrochemical detection. Ethanol (3.0 g/kg, i.p.) stimulated striatal AA release to more than 200% above the baseline. dl -Fenfluramine (20 mg/kg, i.p. or 40 mug/rat, i.c.v.), 10 min before ethanol administration, markedly inhibited ethanol-induced AA release. A similar result was also observed following dl -5-HTP (100 mg/kg, i.p.) administration. However, fluoxetine (10, 30 mg/kg, i.p.) showed no antagonistic effect on ethanol-induced AA release. The suppressing effect of dl -fenfluramine and dl -5-HTP on ethanolinduced AA release could be reversed by the 5-HT receptor antagonist cyproheptadine (10 mg/kg, s.c.). All these drugs had no effect on basal AA release. The results give a first evidence for the involvement of central serotonergic system, and suggest that differential activities may exist between dl -fenfluramine, dl -5-HTP and fluoxetine in regulating ethanol-induced AA release in rat striatum.

Effect of naloxone on morphine-induced changes in striatal dopamine metabolism and glutamate, ascorbic acid and uric acid release in freely moving rats

Recent findings have shown that systemic morphine increases extracellular dopamine (DA), dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA), ascorbic acid (AA) and uric acid concentrations in the striatum of freely moving rats. The morphine-induced increase in DA oxidative metabolism is highly correlated with that of xanthine. In the present study, we evaluated the effects of subcutaneous (s.c.) naloxone (1 mg/kg) on morphine-induced changes in DA, DOPAC, HVA, 5-hydroxyindoleacetic acid (5-HIAA), AA, uric acid and glutamate in the striatum of freely moving rats using microdialysis. Dialysates were assayed by high performance liquid chromatography with electrochemical detection or (glutamate) ultraviolet detection. Morphine (5–20 mg/kg) given s.c. increased DA, DOPAC+HVA, 5-HIAA, AA and uric acid and decreased glutamate dialysate concentrations over a 3 h period after morphine. Morphine (1 mM), given intrastriatally, did not affect all the above parameters, with the exception of an early short-lasting decrease in AA concentration. Naloxone antagonised all morphine-induced changes with the exception of AA increase and glutamate decrease in dialysate concentrations. Systemic or intrastrial (0.2–2 mM) naloxone increased AA and decreased glutamate dialysate concentrations. When given intranigrally, morphine (1 mM) increased DOPAC+HVA, AA and uric acid and decreased glutamate dialysate concentrations over a 2 h period after morphine; DA and 5-HIAA concentrations were unaffected. These results suggest that: (i) morphine increases striatal DA release and 5-hydroxytryptamine oxidative metabolism by a μ-opioid receptor-mediated mechanism mainly at extranigrostriatal sites; (ii) morphine increases DA and xanthine oxidative metabolism and affects glutamate and AA release by a μ-opioid receptor mediated mechanism acting also at nigral sites; and (iii) a μ-opioid receptor-mediated mechanism tonically controls at striatal sites extracellular AA and glutamate concentrations.

5-HT 1A receptors mediate inhibition of ethanol-induced ascorbic acid release in rat striatum studied by microdialysis

Our previous study showed that the serotonergic system was involved in the ethanol-induced striatal ascorbic acid release in rat. In the present study, the 5-HT 1A agonists and antagonists were used to analyze the possible mechanism of ethanol-induced ascorbic acid release in rat striatum. The results showed that ethanol (3.0 g/kg, i.p.) significantly increased striatal ascorbic acid release. Buspirone (5.0 mg/kg, s.c.), a partial agonist of 5-HT 1A receptors, and 8-OH-DPAT (0.5 mg/kg, s.c.), a selective agonist of 5-HT 1A receptors, showed no effect on basal ascorbic acid release in striatum, but both drugs significantly antagonized the ascorbic acid release induced by ethanol in striatum. WAY 100635 (0.5 mg/kg, s.c.), a selective antagonist of 5-HT 1A receptors, affecting neither the basal nor the ethanol-induced ascorbic acid release per se, antagonized the suppressing effect of 8-OH-DPAT on ethanol-induced ascorbic acid release in striatum. This study gives the first evidence that activation of 5-HT 1A receptors is involved in ethanol-induced ascorbic acid release in rat striatum.

Properties of phosphatase from six varieties of apricot relevant to potential use in apricot air‐drying

Apricot phosphatase measured with p‐nitrophenol phosphate as substrate, was present as soluble and membrane‐bound isoforms at levels per gram of tissue generally lower than those found in other fruits, vegetables and cereals. Properties such as substrate affinity, stability at acid pH, heat stability at 50 to 60°C (normal apricot drying temperatures), optimal reaction temperature of 58°C, and reactivity with ascorbic acid polyphosphate favor the use of phosphatase to catalyze the slow release of ascorbic acid over the 36 to 40 h required for air drying. A feasibility trial demonstrated that low levels of ascorbic acid polyphosphate present in the infusion solution (0.5 to 2 g/L) were insufficient to prevent browning, but levels greater than 5 g/L resulted in commercially acceptable dried fruit.

Capillary electrophoresis as analytical method for active ingredient determination in cosmetic matrices

Capillary electrophoresis (CE) has emerged as an important technique applied to analytical chemistry and quality control. In the cosmetic field ascorbic acid is important for soothing, bleaching and for its scavenger activity. Ascorbic acid is responsible for great number of physiological oxidations in electron transfer reactions. Many natural substances have a functional activity which is very difficult to preserve or even to prolong with the requested and expected treatment. This paper reports the study of capillary electrophoresis for the characterization of ascorbic acid as the active ingredient in a new delivery system that is able to preserve stability and to prolong release of ascorbic acid according to the concentration needs of a cosmetic formulation.

Ascorbic acid 2-O-alpha-glucoside-induced redox modulation in human keratinocyte cell line, SCC: mechanisms of photoprotective effect against ultraviolet light B.

We previously reported that the topical application of ascorbic acid 2-O-alpha-glucoside (AA-2G) suppressed the cutaneous inflammation by ultraviolet irradiation in human and guinea pigs (Miyai et al., Nishinihon J. Dermatol., 58, 439-443 (1996)). In this paper, the effect of AA-2G on the lethal damage induced by ultraviolet B (UVB) was studied using a human keratinocyte cell line, SCC, established from squamous cell carcinoma. The photoprotective effect of AA-2G on cytotoxicity of UVB in SCC cells was dose dependent (0.125-1 mM) and more effective than that of ascorbic acid (AsA) at 1 mM. This protection was completely abolished in the presence of an alpha-glucosidase inhibitor, castanospermine, indicating that release of AsA from this derivative was essential for reduction of the actinic injury. AA-2G significantly suppressed cytotoxicities of hydrogen peroxide and superoxide anion produced by xanthine and xanthine oxidase. AA-2G exhibited a preventive effect against the cytotoxicity produced by tert-butylhydroperoxide, an inducer of lipid peroxidation, in the presence of alpha-tocopherol, but not in the absence of alpha-tocopherol. Cytotoxicity of UVB was also effectively reduced by the combination of AA-2G and alpha-tocopherol. In addition, AA-2G reduced UVB-promoted formation of lipid peroxide and accumulation of lipofuscin, which is known to be a complex of cellular proteins and metabolites of lipid peroxide. These data suggest that AA-2G prevents the acute inflammation induced by UVB irradiation partly through scavenging reactive oxygen species and potentiating the antioxidative activity of alpha-tocopherol.

Effect of morphine on striatal dopamine metabolism and ascorbic acid and uric acid release in freely moving rats

Recent ex vivo findings have shown that morphine increases dopamine (DA) and xanthine oxidative metabolism and ascorbic acid (AA) oxidation in the rat striatum. In the present study, we evaluated the effects of subcutaneous daily morphine (20 mg/kg) administration on DA, dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA), AA and uric acid in the striatum of freely moving rats using microdialysis. Dialysates were assayed by high performance liquid chromatography with electrochemical detection. On the first day, morphine administration caused a significant increase in extracellular DA, DOPAC, HVA, AA and uric acid concentrations over a 3 h period after morphine. In all treated rats ( n=7), individual concentrations of DOPAC+HVA were directly correlated with individual AA and uric acid concentrations. Last morphine administration on the 4th day increased DOPAC, HVA, AA and uric acid concentrations but failed to increase those of DA. Individual DOPAC+HVA concentrations were still directly correlated with individual AA and uric acid concentrations. These results suggest that systemic morphine increases both striatal DA release and DA and xanthine oxidative metabolism. Only the former effect undergoes tolerance. The increase in DA oxidative metabolism is highly correlated with that of xanthine. The subsequent enhancement in reactive oxygen species production may account for the increase in extracellular AA.

Endocrine regulation of ascorbic acid transport and secretion in luteal cells.

Luteal ascorbic acid depletion by LH and prostaglandin (PG) F2 alpha is well known, but how such depletion occurs is not. We therefore investigated the nature and regulation of ascorbic acid uptake and depletion in the rat CL and luteal cells. In vivo studies showed that blockade of steroidogenesis by aminoglutethimide prevented ascorbate depletion by LH, but not PGF2 alpha. Also, the time course for half-maximal depletion of ascorbic acid in vivo in response to PGF2 alpha was extremely rapid (2-3 min) compared to that known for LH (60 min). Thus, ascorbate depletion by LH and PGF2 alpha appears to occur by different mechanisms. In luteal cells, ascorbate uptake was energy-, sodium-, and microfilament-dependent with a Michaelis constant (Km) of 33 microM, similar to that reported for other cells. In contrast to findings for other cells, PGF2 alpha was found to be a potent and rapid inhibitor of ascorbate uptake with a half-maximal inhibition (IC50) of about 5 nM in luteal cells. Ascorbate uptake was unaffected by LH, PGE2, glucose, bromo-cAMP, progesterone, phorbol ester, ionomycin, hydrogen peroxide (H2O2), or aminoglutethimide. Also novel was the finding that luteal cell secretion of ascorbic acid was rapidly and potently stimulated by PGF2 alpha (IC50 about 5 nM), an effect mimicked by LH, H2O2, generators of reactive oxygen, calcium ionophore, and cytochalasin B. Basal release of ascorbic acid was energy-dependent, as secretion was blocked by a mitochondrial uncoupler and lowered temperature. Phorbol ester, bromo-cAMP, progesterone, aminoglutethimide, and ouabain had no effect on ascorbic acid secretion in luteal cells. These findings indicate that the secretion of ascorbic acid induced by PGF2 alpha, and possibly LH, may be mediated by calcium, reactive oxygen, and cytoskeletal changes. The ability of PGF2 alpha to inhibit ascorbate transport and to stimulate secretion implicates these processes as the basis for the rapid depletion of ascorbic acid in the CL. Ascorbate depletion by LH is associated with stimulation of steroidogenesis and an increase in ascorbic acid secretion.

Ascorbic acid during cerebral ischemia in newborn piglets.

We measured ascorbic acid (reduced and oxidized) in brain, CSF and blood, before, during and after cerebral ischemia in newborn piglets. Bilateral carotid ligation induced a 54% decrease in cerebral blood flow (p < 0.01) and a 43% decrease in the cerebral metabolic rate of oxygen (p < 0.01). After ischemia and reperfusion, we obtained a 60% decrease (p < 0.01) in total brain ascorbic acid content. CSF ascorbic acid increased during reperfusion: +60% at 30 min (p < 0.001) and +160% at 120 min (p < 0.05). Blood ascorbic acid content did not change. These changes and the absence of massive oxidation of ascorbic acid in brain tissue suggest release of ascorbic acid by the brain during ischemia.

The effects of haloperidol, scopolamine, and MK-801 on amphetamine-induced increases in ascorbic and uric acid as determined by voltammetry in vivo

Amphetamine (which enhances dopaminergic, cholinergic, and glutamatergic activity) increases release of ascorbic acid (AA) and uric acid (UA) in the caudate nucleus. In this study, linear sweep voltammetry with carbon past electrodes was used to investigate the effects of haloperidol (a DA receptor blocker), scopolamine (a muscarinic receptor blocker), and MK-801 (an NMDA receptor blocker) alone and in combination on amphetamine-induced increases in AA and UA in the caudate nucleus. Both scopolamine (0.5 mg/kg, IP) and MK-801 (0.5 mg/kg, IP) significantly reduced amphetamine-induced increases in AA. Also, scopolamine did not affect MK-801-induced reductions of amphetamine-induced increases in AA. Unexpectedly, a subthreshold dose of haloperidol (0.1 mg/kg, IP) potentiated the ability of scopolamine to block amphetamine-induced increases in AA. Therefore, the data suggest that acetylcholine release and subsequent binding to cholinergic receptors in the caudate, are components of amphetamine-induced increases in AA. In addition, scopolamine modulated haloperidol-induced reductions of amphetamine-induced increases in release of UA. Thus, our data demonstrate that cholinergic dopaminergic systems may interact to control release of UA.

Effect of ascorbic acid 2-O-alpha-glucoside on hydrocortisone-induced cataract formation in developing chick embryos: II. Influence on glutathione and lipid peroxide contents in the lens.

In developing chick embryos, hydrocortisone induces cataract formation following a decrease in lens glutathione content but an increase in lipid peroxide content in lens, blood and liver. The preventive effects of ascorbic acid 2-O-alpha-glucoside (AA-2G) on these parameters were compared on cataract formation with those of ascorbic acid (AsA) and ascorbic acid 2-O-phosphate (AA-2P). In these tissues, AA-2G inhibited a decrease in glutathione content and an increase in lipid peroxide content more effectively than either AsA or AA-2P. Various tissues including lens and liver have alpha-glucosidase activity, strongly suggesting that AsA is enzymatically liberated from AA-2G in these tissues. In summary, these results suggest that AA-2G exerts a potent anti-cataract activity via a reduction in oxidative damage through AsA release.

Enhancement of drug release from ethylcellulose microcapsules using solid sodium chloride in the wall

Microcapsules of indomethacin and ascorbic acid were prepared by phase separation of ethylcellulose from cyclohexane using polyisobutylene as a coacervation inducing agent. Different amounts of solid sodium chloride were added to the microcapsule wall in order to alter the porosity of the film and hence to enhance the release of the core materials. The microcapsules prepared were matrix type, coacervates of many drug particles and ethylcellulose. The release of the poorly water-soluble indomethacin was found to be very slow from the ethylcellulose microcapsules, but it was accelerated considerably with increasing amounts of sodium chloride. Indomethacin released through the pores formed when sodium chloride dissolved from the microcapsule film. The release was controlled by the solubility of the weakly acidic drug. Thus a good linearity for the release data was obtained with the Hixson-Crowell cube-root law. The release of the water-soluble ascorbic acid from matrix-type microcapsules was observed to be incomplete and strongly dependent on the core/wall ratio of the microcapsules. The release of ascorbic acid accelerated in some degree as a function of sodium chloride from the microcapsules of higher core to wall ratio, but the enhancement in drug release was quite minimal with the thicker walled ones. Sodium chloride particles acted as pore formers only at the surface of the inhomogeneous microcapsule matrices. The release of the drug was considered to be diffusion controlled having a biphasic release profile against the square root of time.

A cholinergic input to the substantia nigra pars compacta increases striatal dopamine metabolism measured by in vivo voltammetry

3,4-Dihydroxyphenylacetic acid (DOPAC) and ascorbic acid (AA) were measured by differential pulse voltammetry in the neostriatum of anesthetized rats. Physostigmine (2.3 nmol) applied into the substantia nigra pars compacta (SNc), increased DOPAC concentration in the ipsilateral neostriatum, but did not modify AA levels. The largest increase of striatal DOPAC (37 ± 8%above basal) was observed when physostigmine was applied at less than 0.5 mm from SNc, and decreased with increasing distance of the injection site from the pars compacta region. Chemical stimulation of the pedunculopontine tegmental nucleus (PPN) with kainic acid (2.3 nmol) increased both DOPAC and AA concentration in the ipsilateral neostriatum. Pretreatment with the muscarinic antagonist scopolamine (5 mg/kg, i.p.) inhibited the increase of striatal DOPAC from 20 to 70 min after kainic acid injection into the PPN, whereas the increase of AA was reduced from 90 to 160 min. By contrast, the nicotinic antagonist mecamylamine (4 mg/kg, i.p.) did not inhibit neither DOPAC nor AA increase elicited by the chemical stimulation of PPN. These results support the existence of cholinergic neurotransmission within the SNc that increases the firing rate of nigrostriatal dopaminergic neurons, enhancing dopamine turnover in neostriatum without changes in AA release. They also suggest that the PPN could be the origin of cholinergic afferents to the SNc that modulate the activity of dopaminergic neurons, through activation of muscarinic cholinergic receptors. Finally, the activation of a multisynaptic loop involving a cholinergic pathway which modulates the activity of the glutamatergic corticostriatal neurons is postulated to explain the increase of AA in neostriatum observed after PPN stimulation.

Enzymatic Browning Control in Potato with Ascorbic Acid‐2‐Phosphates

ABSTRACTTreated potato samples were evaluated for browning by tristimulus colorimetry and for browning inhibitor uptake by HPLC. Treatment effectiveness was greatly improved by reducing pH to 2.0 with phosphoric acid to inhibit endogenous acid phosphatase and by using combinations of ascorbic acid (AA), AA‐2‐phosphate and AA‐2‐triphosphate to provide for gradual release of AA at treated surfaces. Treatment with dips containing the AA‐2‐phosphates extended storage life of potato dice and pre‐peeled potatoes by 5‐7 days over that obtained with conventional browning inhibitor formulations but induced some leakage at cut surfaces.

Collagen Synthesis in Human Skin Fibroblasts is Stimulated by a Stable Form of Ascorbate, 2-O-α-D-Glucopyranosyl-L-Ascorbic Acid

We evaluated the effect of 2-O-α-D-glucopyranosyl-L-ascorbic acid (AA-2G) on collagen synthesis in cultured human skin fibroblasts and on proliferation of fibroblasts. At concentrations of 0.1–0.5 mmol/L, AA-2G effectively stimulated collagen synthesis with an effectiveness comparable to that of L-ascorbic acid. On the other hand, 6-O-α-D-glucopyranosyl-L-ascorbic acid showed a weak effect. The stimulation of collagen synthesis by AA-2G was attenuated by the addition of a collagen synthesis inhibitor, L-azetidine 2-carboxylic acid, in a dose-dependent manner. In addition, AA-2G-induced stimulation of collagen synthesis could be completely inhibited by the addition of castanospermine, an inhibitor of neutral α-glucosidase. Relatively high α-glucosidase activity, which would contribute to release of ascorbic acid from AA-2G, could be detected in the lysate of cultured fibroblasts. The stimulatory activity of AA-2G on collagen synthesis was observed after 5 d in culture, whereas L-ascorbic acid tended to lose its stimulatory activity. Continuous supplementation of AA-2G (0.25 mmol/L) to culture medium for 24 d enhanced the cell growth four times that of the control. These results indicate that AA-2G is gradually cleaved by the cellular α-glucosidase to release L-ascorbic acid, which adequately stimulates collagen synthesis and proliferation of human skin fibroblasts.