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PubMed2005

Vitamin C content and antioxidant activity of the fruit and of the Ayurvedic preparation of Emblica officinalis Gaertn.

Emblica officinalis Gaertn. is one of the most important plants of Ayurved, the traditional Indian medicine. In this ancient medicine, the fruit of Emblica officinalis is processed according to a method named "Svaras Bhavana", whereby the therapeutic potential of the plant is enhanced by treating the main herb with its own juice. For many years, the activity of the fruits was attributed to the high content of ascorbic acid; however, this has recently been questioned. The aim of the paper is to clarify this matter. A reliable and feasible HPLC method with diode array detection has been developed for the determination of ascorbic acid in Emblica fruit and particularly in Emblica fruit processed according to the Ayurvedic method. The antioxidant effects have also been evaluated in comparison to the real levels of Vitamin C by different antioxidant tests. The data obtained show that the Emblica fruit contains ascorbic acid (0.4%, w/w), and that the Ayurvedic method of processing increases the healthy characteristics of the fruit thanks to a higher antioxidant activity and a higher content of ascorbic acid (1.28%, w/w). It has also been found that Vitamin C accounts for approximately 45-70% of the antioxidant activity.

Antioxidants↗
PubMed1986

Alternative drug therapy for asthma.

Individualized management of asthma requires consideration of single or combined pharmacologic alternatives. This article reviews experimental and clinical data on the efficacy, safety, mode of action, and therapeutic indications for cromolyn and related inhalational compounds; ketotifen; alpha-adrenergic blockers; calcium-channel blockers; nonsteroidal anti-inflammatory drugs; and such diverse agents as immunosuppressive drugs, ether, alcohol, ascorbic acid, and other nutritional substances.

Adrenergic alpha-Antagonists↗
PubMed1986

Unani Joshandah drugs for common cold, catarrh, cough and associated fevers.

Joshandah, polypharmaceutical herbal preparations, are used in the form of a sweetened decoction for the treatment of common cold, catarrh, cough and associated fevers in Unani (Greco-Arab) medicine. The rationale of their therapeutic efficacy is discussed in the light of reported chemico-pharmacological properties of the ingredients.

Ascorbic Acid↗
PubMed1999

Vitamin C supplementation and common cold symptoms: factors affecting the magnitude of the benefit.

Placebo-controlled trials have shown that vitamin C supplementation decreases the duration and severity of common cold infections. However, the magnitude of the benefit has substantially varied, hampering conclusions about the clinical significance of the vitamin. In this paper, 23 studies with regular vitamin C supplementation (> or = 1 g/day) were analyzed to find out factors that may explain some part of the variation in the results. It was found that on average, vitamin C produces greater benefit for children than for adults. The dose may also affect the magnitude of the benefit, there being on average greater benefit from > or = 2 g/day compared to 1 g/day of the vitamin. In five studies with adults administered 1 g/day of vitamin C, the median decrease in cold duration was only 6%, whereas in two studies with children administered 2 g/day the median decrease was four times higher, 26%. The trials analyzed in this work used regular vitamin C supplementation, but it is conceivable that therapeutic supplementation starting early at the onset of the cold episode could produce comparable benefits. Since few trials have examined the effects of therapeutic supplementation and their results have been variable, further therapeutic trials are required to examine the role of vitamin C in the treatment of colds.

Adult↗
PubMed2004

[Study of the antioxidant drug "Karinat" in patients with chronic atrophic gastritis].

A randomized double blind placebo-controlled trial of the drug karinat was carried out in patients with chronic multifocal atrophic gastritis. Karinat contains beta-carotene 2.5 mg, alpha-tocopherol 5 mg, ascorbic acid 30 mg and garlic powder 150 mg per tablet. Out of 66 patients, 34 received karinat, 32--placebo. Both karinat and placebo were administered for 6 months, one tablet twice a day. Karinat therapy improved digestion, the fibrogastroscopic pattern of mucosa, inhibited Helicobacter pylori infection, stimulated stomach activity, mitigated intestinal metaplasia and interfered with the epithelial proliferation of gastric mucosa. These therapeutic effects were more pronounced in the study group. On the whole, the effectiveness of the drug was significantly higher (29%). Karinat should be recommended for the management of chronic atrophic gastritis, a precursor of stomach cancer.

Anticarcinogenic Agents↗
PubMed1983

Altered arachidonic acid synthesis and lipid peroxidation in diabetes mellitus: possible roles in leukocyte dysfunction and other cellular defects.

Hyperglycemic diabetics are prone to unusual or especially severe infections; at the cellular level, diabetic polymorphonuclear leukocytes (PMNs) show defects in several antimicrobial functions. However, the basis for these defects is unknown, and they may not be fully ascribable to hyperglycemia, hypoinsulinemia or acidosis alone. Recently, it has been shown that several important PMN functions may be mediated (at least in part) by metabolites of arachidonic acid synthesized via the lipoxygenase pathway, especially arachidonate hydroperoxides and leukotriene (LT) B4. We speculate that synthesis of these mediators may be deficient in severely hyperglycemic diabetics (fasting plasma glucose greater than 250-300 mg/dl) due to deficiencies of substrate (arachidonic acid) synthesis and release. Such defects might be expected since, in animal studies, severe insulin lack and glucagon excess inhibit the desaturation of precursor fatty acids to arachidonic acid. On the other hand, whereas low levels of lipid peroxides or their derivatives may be required in certain cells for normal function, excessive levels of such compounds also are detrimental to cellular function and could play a role as well in the complications of milder or partially treated diabetics who manifest high basal insulin levels. For example, cells which may be particularly sensitive to an excess of peroxides include islet beta cells, PMNs and possibly vascular endothelial cells (all of which appear to be deficient in glutathione peroxidase). These observations suggest a role for accumulation of lipid peroxides in the impaired insulin secretion, defective PMN function and possibly endothelial death and increased vascular (retinal, endothelial, and renal) permeability of some milder diabetics. The available data are compatible with the speculation that in partially treated or lesser degrees of hyperglycemia, increased arachidonate synthesis and excessive lipid peroxidation may be present. Although it remains to be established that all of the results from experimentally-induced diabetics can be extrapolated to humans, these findings suggest that the cell damage attendant upon peroxide generation might be susceptible to prophylactic treatment with anti-oxidants such as alpha-tocopherol or ascorbic acid. In the more severe or later stages of hyperglycemia, a deficiency of lipoxygenase-derived products may supervene; dietary modifications designed to increase essential fatty acid availability might present a unique ancillary therapeutic approach at this stage of diabetes.

Arachidonic Acid↗
PubMed1991

Reduced bactericidal activity in neutrophils from scorbutic animals and the effect of ascorbic acid on these target bacteria in vivo and in vitro.

Actinomycetes, involved in oral and periodontal diseases, cause serious infections in immunocompromised hosts. Severely scorbutic guinea pig leukocytes killed only 12% of phagocytosed actinomycetes, had distorted nuclear morphology, had 16 times less ascorbate, and had no chemotactic responses in vitro. Ascorbate reversed these indices and also prevented nitrosamine formation by oral organisms. Degranulating leukocytes release lactoferrin and ascorbate that chelate iron, essential for microorganisms. Ascorbic acid, 2,2'-bipyridine and 1,10-phenanthroline were bactericidal to several bacterial pathogens at millimolar concentrations. Iron alone reversed this effect. In in vivo experiments an Actinomyces viscosus monoflora was implanted in rhesus monkeys. Plaque and serum samples showed decreased (by six orders of magnitude) bacterial counts and decreased actinomycete antibody titers in animals given 1 g ascorbate/d. Removing ascorbate returned counts and titers to preascorbate concentrations. Fifteen marmosets, receiving twice daily topical applications of ascorbate or water, had comparatively lower gingival, calculus, and plaque indices and only slightly lowered actinomycete counts.

Actinomyces viscosus↗
PubMed1998

Lung lining fluid antioxidants in male broilers: age-related changes under thermoneutral and cold temperature conditions.

The purpose of this study was to determine age-related changes in lung lining fluid antioxidants in broilers reared under thermoneutral or cold temperature conditions. Male broilers (Cobb 500) were placed in floor pens within environmental chambers and fed a standard commercial starter diet. The thermoneutral Control chamber was maintained at 32, 30, 27, and 22 to 25 C for Weeks 1, 2, 3, and 4 to 7, respectively, whereas temperature in the Cold chamber was lowered to 18 C during Week 3 and maintained between 15 and 18 C for the rest of the study. At 2, 4, and 7 wk, four to six birds per chamber were selected randomly. The lungs were lavaged with heparinized saline (2 mL/g lung) to obtain lung lining fluid. Antioxidants [reduced (GSH), oxidized (GSSG), and total (TGSH) glutathione, uric acid, ascorbic acid, and alpha- and gamma-tocopherol] in lung lining fluid were determined by HPLC; protein was determined colorimetrically. In Controls, levels of alpha- and -gamma-tocopherol, uric acid, and GSH in lung lining fluid decreased between 2 and 7 wk of age. Birds in the Cold chamber exhibited higher protein, a higher GSSG:TGSH ratio, and a decrease in ascorbic acid (7 wk) in lung lining fluid relative to Controls. Lung lining fluid antioxidants were not correlated with antioxidants in plasma. To determine the effect of vitamin E supplementation on lung lining fluid antioxidants, birds were given a supplement of 200 IU alpha-tocopherol per day for 7 d. Alpha-tocopherol supplementation elevated alpha-tocopherol levels in lung lining fluid, but lowered ascorbic acid, GSH, and GSSG and had no effect on uric acid in lung lining fluid. The results of this study suggest that antioxidant protection in lung lining fluid may diminish with age, that cold conditions in this study produced an oxidative stress in lung lining fluid in broilers, and that oral supplementation of alpha-tocopherol elevated lung lining fluid alpha-tocopherol.

Aging↗
PubMed2006

Ascorbic acid differentially modulates the induction of heme oxygenase-1, NAD(P)H:quinone oxidoreductase 1 and glutathione S-transferase Ya by As(3+), Cd(2+) and Cr(6+).

The induction of phase II drug metabolizing enzymes serves as a detoxification mechanism for many mutagens, carcinogens and other toxic compounds. Specifically, NAD(P)H:quinone oxidoreductase 1 (Nqo1) and glutathione S-transferase Ya subunit (Gst ya) are key enzymes involved in cellular defense against reactive forms of oxygen and the inhibition of carcinogenesis. As(3+), which induces these enzymes, has been proven to have a role in the treatment of acute promyelocytic leukemia. Ascorbic acid (AA) potentiates the anticancer effect of As(3+) and thus it is expected that this antioxidant will have a paradoxical effect on the ability of heavy metals, specifically As(3+), to induce Nqo1 and Gst ya. We have shown that As(3+) and Cd(2+) induce heme oxygenase-1 (HO-1), Nqo1 and Gst ya mRNA levels but Cr(6+) decreases Nqo1 and Gst ya mRNA. Surprisingly, AA superinduced the induction of HO-1, Nqo1 and Gst ya mRNA by As(3+), while inhibiting the induction of HO-1 mRNA by Cd(2+) and Cr(6+). Hence, it is tempting to speculate that AA may potentiate the therapeutic efficacy of As(3+) by enhancing the expression of HO-1, Nqo1, and Gst ya while acting as a potent antioxidant.

Animals↗
PubMed2002

Advanced glycation end-products induce apoptosis of bovine retinal pericytes in culture: involvement of diacylglycerol/ceramide production and oxidative stress induction.

One of the earliest changes observed in retinal microvessels in diabetic retinopathy is the selective loss of intramural pericytes. We tested the hypothesis that AGE might be involved in the disappearance of retinal pericytes by apoptosis and further investigated the signaling pathway leading to cell death. Chronic exposure of pericytes to methylglyoxal-modified bovine serum albumin (AGE-BSA) (3 microM) leads to a 3-fold increase of apoptosis (8.9 +/- 1.1%), associated with an increase in cellular ceramide (185 +/- 12%) and diacylglycerol (194 +/- 9%) levels. Ceramide formation was almost inhibited (95%) by an acidic sphingomyelinase inhibitor, desipramine (0.3 microM). Dual inhibition of ceramide (95%) and diacylglycerol (80%) production was observed with a phosphatidylcholine-phospholipase C inhibitor, D609 (9.4 microM). Taken together, these results suggest activation of phosphatidylcholine-phospholipase C coupled to acidic sphingomyelinase. However, both inhibitors only partially protected pericytes against apoptosis, suggesting another apoptotic pathway independent of diacylglycerol/ceramide production. Treatments with various antioxidants completely inhibited pericyte apoptosis, suggesting oxidative stress induction during this apoptotic process. Inhibition of diacylglycerol/ceramide production by N-acetyl-L-cysteine suggests that oxidative stress acts upstream of the two metabolic pathways. AGE treated with metal chelators were also able to induce pericyte apoptosis, suggesting a specific effect of AGE on intracellular oxidative stress independent of redox-active metal ions bound to AGE. In conclusion, these results identify new biochemical targets involved in pericyte loss, which can provide new therapeutic perspectives in diabetic retinopathy.

Adrenergic Uptake Inhibitors↗
PubMed2000

Enhanced invasion of Tax-expressing fibroblasts into the basement membrane is repressed by phosphorylated ascorbate with simultaneous decreases in intracellular oxidative stress and NF-kappa B activation.

Invasion of rat fibroblastic cells Rat-1 through Matrigel was shown to be promoted by transfection with tax gene of human T-cell leukemia virus type 1. We found that an oxidation-resistant type of vitamin C (Asc), Asc-2-O-phosphate (Asc2P), inhibited the invasion of the tax-transfected Rat-1 cells (W4 cells). Intracellular Asc (Ascin), after enzymatic dephosphorylation of administered Asc2P, was more abundant in W4 cells than in Rat-1 cells, and the ratio of dehydroascorbic acid versus Asc was increased in W4 cells but scarcely in Rat-1 cells, according to the enhanced level of intracellular reactive oxygen species (ROSin) in W4 cells. Asc2P notably repressed the increases in both ROSin and secretion of matrix metalloproteases (MMPs), but did not affect Tax protein expression in tax-transfectants. NF-kappa B activation, as evidenced by its translocation to the nucleus in W4 cells, was also repressed by Asc2P. Thus, the tax-promoted invasion together with the enhanced production of MMPs occurred with NF-kappa B activation and the increase in ROSin, both of which were effectively reduced by Asc2P. These findings indicate the therapeutic efficacy of Ascin-enriching agents for the prevention against tumor invasion in which ROSin plays a major role.

Animals↗
PubMed1985

Ascorbic acid: a putative biochemical marker of irreversible neurologic functional loss following spinal cord injury.

The development of permanent paraplegia in spinal injured cats is accompanied by a large progressive decline in total ascorbic acid (AA) and a transient increase in oxidized (AAox) ascorbate. Since AA is involved in a variety of processes required for normal central nervous system (CNS) performance we suggested that such large ascorbate loss may contribute to derangements in spinal cord function following injury. We now demonstrate that methylprednisolone (15 mg/kg) and naloxone (10 mg/kg), two treatments that preserve neurologic function in this model, rapidly block deteriorating ascorbate status. Naloxone at 1 mg/kg, a treatment providing no therapeutic benefit, has no protective effect on ascorbate. The results strongly support the hypothesis that loss of ascorbate homeostasis reflects irreversible loss of neurologic function following spinal cord injury.

Animals↗
PubMed1995

Antiparkinsonian therapies and brain mitochondrial complex I activity.

Alterations in complex I activity, one of the enzymatic units of the mitochondrial respiratory chain, have been demonstrated in different tissues from patients with Parkinson's disease (PD). Subsequently, we showed that the chronic administration of levodopa can cause alterations in mitochondrial respiratory chain activity in rats, which suggests that the observed deficit in complex I activity in PD might be, at least in part, related to chronic levodopa therapy. Our study assessed the in vitro effects of different antiparkinsonian agents on complex I activity in rat brain. As previously reported, both levodopa and dopamine inhibit complex I activity in a dose-dependent manner. In contrast, the two major metabolites of dopamine, homovanillic acid and 3,4-dihydroxyphenylacetic acid as well as 3-O-methyl-dopa, had little or no effect on complex I activities. Bromocriptine, pergolide, trihexyphenidyl, molindone, and clozapine were all without significant inhibitory effects on mitochondrial function. Although vitamin C and deprenyl did not alter complex I activity, they did prevent the inhibitory effect of both levodopa and dopamine on complex I activity. This work indicates that among the different and usual antiparkinsonian agents, only levodopa and dopamine induced reductions in complex I activity. It also indicates that vitamin C and deprenyl are both effective in preventing the levodopa-induced complex I inhibition. This latter finding provides further support to the use of antioxidants and monoamine oxidase inhibitors as therapeutic strategies in attempts to slow the progression of PD.

Animals↗
PubMed2000

How urine analysis reflects oxidative stress--nitrotyrosine as a potential marker.

Enhanced oxidant stress involved in the pathogenesis of cardiovascular (heart failure, atherosclerosis, ischemia-reperfusion injury), neurodegenerative (M. Alzheimer), metabolic (hypercholesterolemia, diabetes) and inflammatory disorders is mimicked by non-intermittent therapy with nitrovasodilators. We used this latter therapy model to study urinary 3-nitrotyrosine (n-tyr) excretion as a potential biomarker that may reflect the enhanced generation of reactive oxygen species. Namely, free or protein-bound n-tyr is formed in the organism by nitration of tyrosine (residues) via peroxynitrite (reaction product of NO&z.ccirf; and O(2)(-)&z. ccirf;). Free n-tyr content was analyzed by gas chromatography in urine obtained from healthy human subjects under a nitrite-limited diet during a two-day non-intermittent transdermal administration of glyceroltrinitrate (GTN; 0.4 mg/h) with or without vitamin C (Vit-C; 55 microg/kg/min) as antioxidant. Concomitant with the development of complete vascular tolerance (loss of dilator action), a progressive increase in urinary n-tyr excretion (up to 186+/-9 microg/day) was demonstrated in volunteers given GTN only. In contrast, when Vit-C was added, the GTN-induced increases in urinary n-tyr content were significantly suppressed (up to 130.20+/-6.91 microg/day), whereas Vit-C alone even decreased urinary n-tyr content (down to 34.00+/-5.66 microg/day), which was below control values (56.0+/-3.4 microg/day). Thus, urinary n-tyr may serve as a biomarker to detect changes in oxidant stress and thereby to evaluate the efficacy of therapeutic interventions aimed at reducing oxidant stress under various pathophysiological conditions.

Adult↗
PubMed2005

Role of antioxidants in atherosclerosis: epidemiological and clinical update.

Low density lipoprotein (LDL) oxidative modification in the vascular wall seems to be a key factor in atherosclerosis development. Oxidised LDLs might recruit monocytes and favour their transformation into foam cells through a receptor-mediated intake (scavenger pathway). Moreover oxidised LDLs show cytotoxic potential which is probably responsible for endothelial cell damage and macrophage degeneration in the atherosclerotic human plaque. Following the oxidation hypothesis of atherosclerosis the role of natural antioxidants, i.e. Vitamin C, Vitamin E and carotenoids, has been investigated in a large number of epidemiological, clinical and experimental studies. Animal studies indicate that dietary antioxidants may reduce atherosclerosis progression, and observational data in humans suggest that antioxidant vitamin ingestion is associated with reduced cardiovascular disease, but the results of randomised controlled trials are mainly disappointing. It has been suggested that natural antioxidants may be effective only in selected subgroups of patients with high levels of oxidative stress or depletion of natural antioxidant defence systems. The favourable effects shown by some studies relating antioxidant dietary intake and cardiovascular disease, may have been exerted by other chemicals present in foods. Flavonoids are the ideal candidates, since they are plentiful in foods containing antioxidant vitamins (i.e. fruits and vegetables) and are potent antioxidants. Tea and wine, rich in flavonoids, seem to have beneficial effects on multiple mechanisms involved in atherosclerosis. Future studies should probably select patients in a context of high-oxidative stress / low-antioxidant defence, to verify if antioxidants may really prove useful as therapeutic anti-atherosclerotic agents.

Animals↗
PubMed1997

[Pharmacological therapy of complicated Parkinson's disease].

The progression of Parkinson's disease, and the increase in the time under therapy with levodopa of this disease, leds to development of several complications, including loss of efficacy of the therapy, motor fluctuations, dyskinesias, psychiatric disorders, etc. These complications cause serious limitations to the management of the advanced disease. This article reviews the current status of the therapeutic approaches to the management of complicated Parkinson's disease.

Antiparkinson Agents↗
PubMed2006

Involvement of reactive oxygen species in the action of ciprofloxacin against Escherichia coli.

Ciprofloxacin is an important and commonly used member of the fluoroquinolone group of antibiotics. Ciprofloxacin inhibits DNA topoisomerase II and DNA topoisomerase IV activities, eventually leading to bacterial cell death. In addition, an increase of reactive oxygen species in the bacterial cells in response to ciprofloxacin has been shown. We investigated the role of reactive oxygen species in the antibacterial action of ciprofloxacin by studying the effects of different antioxidant compounds on ciprofloxacin susceptibility of Escherichia coli. Among the antioxidants checked, glutathione and ascorbic acid provided substantial protection against ciprofloxacin. The involvement of superoxide anion (O2-) and hydrogen peroxide (H2O2) in the antibacterial action of ciprofloxacin was analyzed using superoxide dismutase, catalase, and alkyl hydroperoxide reductase knockout strains of E. coli. The effects of multicopy sod genes on ciprofloxacin susceptibility of E. coli were also analyzed. On the basis of our results, we conclude that O2- and H2O2 may be involved in antibacterial action of ciprofloxacin. Our findings that glutathione gave protection against other fluoroquinolones and not against nonfluoroquinolone antibiotics imply that reactive oxygen species may have a similar role in the antibacterial action of all these fluoroquinolones and that glutathione-mediated protection is not a general phenomenon but specific to fluoroquinolones. These observations are of significance, as fluoroquinolones are important antibiotics with immense therapeutic value, and the effectiveness of treatment by these drugs may be affected by dietary intake and cellular levels of these antioxidants.

Anti-Infective Agents↗