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PubMed1988

Reduction of hexavalent chromium by ascorbic acid in rat lung lavage fluid.

The reduction of hexavalent chromium [chromium(VI)] in lung lavage fluids, microsomal (S-9) fractions of lung and liver tissues, erythrocyte lysates and plasma prepared from adult rats was examined at pH 7.4 (37 degrees C). Specific reducing capacity, which was defined as the amount of chromium(VI) reduced per mg of protein in the test sample, was highest in the lavage fluids. The concomitant trivalent species [chromium(III)] was detected as complexes with some of the lavage components and probably as colloidal hydroxides. By gel filtration analysis and UV spectrometry, ascorbic acid (AsA) was identified as an important reducing factor in the lavage fluids. AsA levels in the lavage fluids were about 38 micrograms/g tissue, corresponding to 12% of total AsA in the intact lungs. The molar ratios of oxidized AsA and reduced chromium(VI) in the lavage samples were about 3:2.3 on an average. On the basis of this molar ratio, the AsA levels in the lavage fluids are equivalent to a reducing capacity of 8.4 micrograms chromium(VI)/g tissue. These results suggest that the lining layers (surfactant layers) of rat lungs provide an AsA-related capacity for protection of the cells against the toxic effects of chromates and probably other oxidants.

Animals↗
PubMed1985

Oxygen toxicity: loss of lung macrophage function without metabolite depletion.

Hyperoxia inhibited concanavalin A stimulated O2- release (respiratory burst) of alveolar macrophages obtained by bronchoalveolar lavage from rats. After 36 h of normobaric 100% O2, a partial reversal (48%) of the inhibition was produced by addition of glucose. Since oxidant-induced, reversible NADPH depletion correlates with reversible inhibition of the respiratory burst, intracellular NADPH was assayed to determine whether irreversible inhibition of the respiratory burst was related to persistent changes in this metabolite. The cellular concentrations of ATP, glutathione, and ascorbate were also measured. After 36 h of hyperoxia, NADPH concentration in alveolar macrophages rose slightly while ATP and glutathione content remained at control levels. Ascorbate levels fell significantly but were not responsible for respiratory burst inhibition. Thus, irreversible loss of cellular function in hyperoxia is not due to persistent alterations in these metabolites. Significant amounts of both glutathione and ascorbate were found in extracellular fractions of lung washings, indicating high concentrations in the aqueous subphase in the lung fluid lining. There was no change in total content of these extracellular antioxidants following O2 exposure.

Animals↗
PubMed1984

Nerve staining with leucomethylene blue: an experimental study.

Identification and preservation of the facial nerve during extirpative and reconstructive surgery represents a challenge even for the experienced surgeon. We present an experimental intraoperative technique for staining the facial nerve and its branches that is safe, accurate, and inexpensive. Leucomethylene blue is injected into the precise region of the facial nerve. Staining of the surrounding tissues is efficiently reduced by irrigation with ascorbic acid solution, leaving only the facial nerve stained. This technique has been encouraging in rabbits, and with additional experience, we anticipate its use for intraoperative staining of the facial nerve in humans.

Animals↗
PubMed1983

A comparative study of the therapeutic effect of dithranol cream 0.1% and 0.25% with that of dithranol stylus 0.1% and 0.2% in the treatment of psoriasis.

In Dithranol cream the oily phase is emulsified with an aqueous phase to make the preparation more convenient to apply. The cream also contains ascorbic acid as an antioxidant, which protects dithranol against atmospheric oxidation, thus increasing its stability. A stylus containing dithranol, ol. cacao, paraffin and vaselinum has been used as a comparative drug. The stylus is routinely used in this clinic. Sixty patients with stable psoriasis were pre-assigned into two treatment groups, receiving at random Dithranol cream 0.1%, 0.25% and Dithranol stylus 0.1%, 0.2%, respectively. Both groups started their treatment with the 0.1% preparation once a day for 2 weeks followed by the 0.2% or 0.25% preparations once a day for another 2 weeks. The following laboratory tests: Hb, WBC, Diff, S-ALAT, S-ASAT and S-creatinine were recorded before and after treatment. Staining of clothes was none to slight in 70% (21/30) of the patients using Dithranol stylus 0.2%, and 80% (24/30) in the patients using Dithranol cream 0.25%. The sensation of burning was none to slight in 83% (25/30) of the patients and skin discolouration was none to slight in approximately 80% (24/30) of the patients using the Dithranol stylus 0.2% and Dithranol cream 0.25% preparations. Both groups showed significant improvement in all effect-variables after 2 and 4 weeks' treatment compared to initial. The results are over all better after 4 weeks' treatment than after 2. No abnormal values due to dithranol treatment could be found in the laboratory tests.

Adolescent↗
PubMed1975

The role of vitamins in hemostasis.

The physiological mechanism to prevent and control abnormal bleeding is dependent on three vitamins (C, K, and Q). Two of these are unequivocally established as essential for hemostasis while the existence of the third (Q) is supported by experimental evidence and by clinical and therapeutic observations (Quick 1972; Quick 1974). The interrelationship of these three vitamins has remained moot except for clue observations. Both vitamins C and K have a key structure in their molecules which supplies a redox mechanism, ascorbic acid and 2-methyl, 1,4-naphthoquinone, respectively. Both vitamins are concerned with growth. Lack of vitamin C, which clinically is the basic defect of scurvy, does not appear to cause a defect in blood coagulation while vitamin K affects the clotting mechanism by being essential for the production of four distinct clotting factors: prothrombin, factors VII, IX and X. In this presentation an attempt is made to correlate the action of the vitamin K-dependent clotting factors grouping them in a diagram to show how two systems of thrombin formation exist, one being essentially intrinsic, the second extrinsic requiring tissue thromboplastin and factor VII. The possible interlocking of vitamin Q in this mechanism is presented.

Animals↗
PubMed2002

Bioavailability of a series of novel acylated ascorbic acid derivatives, 6-O-acyl-2-O-alpha-D-glucopyranosyl-L-ascorbic acids, as an ascorbic acid supplement in rats and guinea pigs.

The bioavailability of a series of novel acylated ascorbic acid derivatives, 6-O-acyl-2-O-alpha-D-glucopyranosyl-L-ascorbic acids (6-Acyl-AA-2G), as an ascorbic acid (AA) supplement was investigated in rats and guinea pigs. Oral administration of 6-Acyl-AA-2G to rats resulted in an increase in the plasma AA level. However, the intact form was not detectable in the plasma by high-performance liquid chromatography, indicating its hydrolysis through the process of absorption. After an intravenous injection to rats of 6-Octa-AA-2G as a representative derivative, the intact form rapidly disappeared from the plasma, being followed by a prolonged and marked elevation of the plasma AA level. Various tissue homogenates from guinea pigs were examined for their releasing activity of AA, 2-O-alpha-D-glucopyranosyl-L-ascorbic acid (AA-2G) and 6-O-acyl-AA from 6-Acyl-AA-2G. High activity was observed in the small intestine. These hydrolytic activities to AA and 6-O-acyl-AA were completely inhibited by castanospermine, an alpha-glucosidase inhibitor, and AA-2G was observed as the only resulting hydrolysate, suggesting the participation of alpha-glucosidase and esterase in the in vivo hydrolysis of 6-Acyl-AA-2G. 6-Octa-AA-2G was found to exhibit an obvious therapeutic effect in scorbutic guinea pigs from its repeated oral administration. These results indicate that 6-Acyl-AA-2G is a readily available source of AA activity in vivo, and may be useful as an effective pharmacological agent and as a promising food additive.

Animals↗
PubMed1999

Interaction of antioxidants and their implication in genetic anemia.

The generation of reactive oxygen species (ROS) is a steady-state cellular event in respiring cells. Their production can be grossly amplified in response to a variety of pathophysiological conditions such as inflammation, immunologic disorders, hypoxia, hyperoxia, metabolism of drug or alcohol, exposure to UV or therapeutic radiation, and deficiency in antioxidant vitamins. Uncontrolled production of ROS often leads to damage of cellular macromolecules (DNA, protein, and lipids) and other small antioxidant molecules. A number of major cellular defense mechanisms exist to neutralize and combat the damaging effects of these reactive substances. The enzymic system functions by direct or sequential removal of ROS (superoxide dismutase, catalase, and glutathione peroxidase), thereby terminating their activities. Metal binding proteins, targeted to bind iron and copper ions, ensure that these Fenton metals are cryptic. Nonenzymic defense consists of scavenging molecules that are endogenously produced (GSH, ubiquinols, uric acid) or those derived from the diet (vitamins C and E, lipoic acid, selenium, riboflavin, zinc, and the carotenoids). These antioxidant nutrients occupy distinct cellular compartments and among them, there are active recycling. For example, oxidized vitamin E (tocopheroxy radical) has been shown to be regenerated by ascorbate, GSH, lipoic acid, or ubiquinols. GSH disulfides (GSSG) can be regenerated by GSSG reductase (a riboflavin-dependent protein), and enzymic pathways have been identified for the recycling of ascorbate radical and dehydroascorbate. The electrons that are used to fuel these recycling reactions (NADH and NADPH) are ultimately derived from the oxidation of foods. Sickle cell anemia, thalassemia, and glucose-6-phosphate-dehydrogenase deficiency are all hereditary disorders with higher potential for oxidative damage due to chronic redox imbalance in red cells that often results in clinical manifestation of mild to serve hemolysis in patients with these disorders. The release of hemoglobin during hemolysis and the subsequent therapeutic transfusion in some cases lead to systemic iron overloading that further potentiates the generation of ROS. Antioxidant status in anemia will be examined, and the potential application of antioxidant treatment as an adjunct therapy under these conditions will be discussed.

Anemia↗
PubMed1997

Metabolic and vascular factors in the pathogenesis of diabetic neuropathy.

Reduced nerve perfusion is an important factor in the etiology of diabetic neuropathy. Studies in streptozotocin-induced diabetic rats show that nerve conduction velocity (NCV) and blood flow deficits are corrected by treatment with vasodilator drugs, with angiotensin II and endothelin-1 antagonists being particularly important. The AT1 antagonist ZD7155 also prevents diabetic deficits in regeneration following nerve damage, indicating that hypoperfusion is an important limitation for nerve repair. Metabolic changes include high polyol pathway flux, increased advanced glycosylation, elevated oxidative stress, and impaired omega-6 essential fatty acid metabolism. Aldose reductase inhibitors (ARIs) restore NCV via their effects on perfusion. ARI action probably depends on blocking the conversion of glucose to sorbitol, thus preventing depletion of vasa nervorum glutathione, an important endogenous free radical scavenger. Free radicals cause vascular endothelium damage and reduced nitric oxide vasodilation. Inhibition of advanced glycosylation and autoxidation (autoxidative glycosylation), major sources of free radicals, by aminoguanidine or transition metal chelators, corrects neurovascular dysfunction. Evening primrose oil supplies gamma-linolenic acid (GLA) to improve vasodilator eicosanoid synthesis in diabetes, correcting nerve blood flow and NCV deficits. Interactions between some of these mechanisms have therapeutic implications. Thus, combined ARI and evening primrose oil treatment produced a 10-fold amplification of NCV and blood flow responses. Similarly, GLA effects are markedly enhanced when given in combination with ascorbate as ascorbyl-GLA. Thus, metabolic abnormalities combine to produce deleterious changes in nerve perfusion that make a major contribution to the etiology of diabetic neuropathy. The potential importance of multi-action therapy is stressed.

Animals↗
PubMed1969

Absorption of therapeutic preparations of iron measured with a whole body counter.

The Oxford Whole Body Counter was used to measure absorption from various therapeutic preparations of iron in five groups of subjects. Succinic acid enhanced absorption of iron when added to a solution of ferrous fumarate, but not when given with tablets of ferrous fumarate or ferrous sulphate. Ferrous fumarate plus ascorbic acid was absorbed better than ferrous fumarate alone but no better than ferrous sulphate. The addition of ascorbic acid and succinic acid to tablets of ferrous sulphate did not enhance absorption significantly.

Anemia, Hypochromic↗
PubMed2005

Vitamins E and C pretreatment prevents ovariectomy-induced memory deficits in water maze.

We investigated whether the pretreatment with vitamins E (alpha-tocopherol) and C (ascorbic acid) would act on ovariectomy-induced memory deficits in Morris water maze tasks. Adult female Wistar rats were divided into three groups: (1) naive (control), (2) sham (submitted to surgery without removal of ovaries) and (3) ovariectomized. Thirty days after surgery, they were trained in the Morris water maze in order to verify ovariectomy effects both on reference and working memory tasks. Results show that ovariectomized rats presented impairment in spatial navigation in the acquisition phase, as well as in the time spent in target quadrant and in the latency to cross over the location of the platform in test session, when compared to naive and sham groups (controls), in the reference memory task. Ovariectomy did not affect performance in the working memory task. Confirming our hypothesis, ovariectomized rats pretreated for 30 days with vitamins E and C had those impairments prevented. We conclude that ovariectomy significantly impairs spatial reference learning/memory and that pretreatment with vitamins E and C prevents such effect. Assuming this experimental memory impairment might mimic, at least in part, the cognitive deficit sometimes present in the human condition of lack of reproductive hormones, our findings lend support to a novel therapeutic strategy, based on vitamins E and C, to cognitive impairments in post-menopausal women.

Animals↗
PubMed2006

Animal models of inherited neuropathies.

PURPOSE OF REVIEW: Mutations in a number of genes have been associated with inherited neuropathies (Charcot-Marie-Tooth or CMT disease). This review highlights how animal models of demyelinating CMT have improved our understanding of disease mechanisms. Transgenic CMT models also allow therapies to be developed in a preclinical setting. RECENT FINDINGS: Rodent models for the most common subtypes of human CMT disease are now available, and two mouse mutants modeling the rare CMT4B subform have lately extended this repertoire. In a peripheral myelin protein 22 kDa (Pmp22) transgenic rat model of CMT1A, administration of a progesterone receptor antagonist reduced Pmp22 overexpression, axon loss and clinical impairments. Dietary ascorbic acid prevented dysmyelination and premature death in a Pmp22 transgenic mouse line. Neurotrophin-3 promoted small fiber remyelination in CMT1A xenografts and sensory functions in CMT1A patients. Gene expression profiling in rodent models of CMT may identify further therapeutical targets. While original classifications distinguish the demyelinating and axonal forms of CMT, recent findings emphasize that axon loss is a common feature, possibly caused by Schwann cell defects rather than demyelination per se. This supports our model that myelination and long-term axonal support are distinct functions of all myelinating glial cells. SUMMARY: Animal models have opened up new perspectives on the pathomechanisms and possible treatment strategies of inherited neuropathies.

Animals↗
PubMed1993

Genitourinary malakoplakia.

Between 1973 and 1991, 13 patients with malakoplakia (MKP) have been diagnosed and treated. The lesions involved all sites in the genitourinary tract; 2 patients had multiple and 11 had single lesions. Treatment was based on 2 criteria: (a) pharmacological treatment with trimethoprim-sulphamethoxazole and/or ascorbic acid and/or bethanechol chloride; (b) excision of the MKP lesion either endoscopically or by open surgery. Two patients died (1 from multiple MKP and the other from a myocardial infarct); the remainder did well. The pathogenic, diagnostic and therapeutic aspects of the disease are discussed.

Aged↗
PubMed1998

Nasal cavity lining fluid ascorbic acid concentration increases in healthy human volunteers following short term exposure to diesel exhaust.

To determine if diesel exhaust (DE) exposure modifies the antioxidant defense network within the respiratory tract lining fluids, a randomized, single blinded, crossover control study using nasal lavage and flexible video bronchoscopy with bronchial and bronchoalveolar lavage was performed. Fifteen healthy, non-smoking, asymptomatic subjects were exposed to filtered air or diluted diesel exhaust (300mg m(-3) particulates, 1.6ppm nitrogen dioxide) for one hour on 2 separate occasions, at least three weeks apart. To examine the kinetics of any DE-induced antioxidant reactions, nasal lavage fluid and blood samples were collected prior to, immediately after, and 5 1/2 hours post exposure. Bronchoscopy was performed 6 hours after the end of DE exposure. Ascorbic acid, uric acid and reduced glutathione (GSH) concentrations were determined in nasal, bronchial, bronchoalveolar lavage and plasma samples. Malondialdehyde (MDA) and protein carbonyl concentrations were determined in plasma and bronchoalveolar lavage samples. Nasal lavage ascorbic acid concentration increased 10-fold during DE exposure [1.02 (0.26-2.09) Vs 7.13 (4.66-10.79) micromol/L(-1)], but returned to basal levels 5.5 hours post-exposure [0.75 (0.26-1.51) micromol/L(-1)]. There was no significant effect of DE exposure on nasal lavage uric acid or GSH concentration. DE exposure did not influence plasma, bronchial wash, or bronchoalveolar lavage antioxidant concentrations and no change in MDA or protein carbonyl concentrations were found. The physiological response to acute DE exposure is an increase in the level of ascorbic acid in the nasal cavity. This response appears to be sufficient to prevent further oxidant stress in the respiratory tract of normal individuals.

Adult↗
PubMed1979

[The effect of rooibos tea on iron absorption].

A study was carried out to determine if rooibos tea (Aspalathus linearis) has a deleterious effect on iron absorption similar to that of ordinary tea (Camellia sinensis). Three groups of volunteers, each consisting of 10 healthy young men comparable with regard to iron status and body dimensions, were studied. After ingestion of 1 muCi 59Fe and 16 mg of elemental iron, group A drank rooibos tea, group B ordinary tea and group C boiled water. Iron absorption was measured 14 days later with a whole body counter. Mean iron absorption after ingestion of rooibos tea, ordinary tea, and water was 7,25%, 1,70% and 9,34% respectively. In contrast to ordinary tea (P less than 0,0001), rooibos tea did not affect iron absorption significantly. The ascorbic acid content of rooibos tea varies between 121,8 and 154,9 mumol/l, depending on the method of preparation. Rooibos tea contains small amounts of iron, magnesium, phosphorus, sodium, chloride and potassium. These findings have practical nutritional and therapeutic implications.

Adult↗
PubMed1986

Treatment of mitochondrial myopathy due to complex III deficiency with vitamins K3 and C: A 31P-NMR follow-up study.

A patient with mitochondrial myopathy due to complex III deficiency who was treated with vitamin K3 (menadiol sodium diphosphate, 40 mg daily) and vitamin C showed clinical improvement. A 1-year study with phosphorus 31 nuclear magnetic resonance (31P-NMR) monitoring has shown that clinical and metabolic improvement was maintained by this therapy; increasing the dose of vitamin K3 to 80 mg daily improved the bioenergetic state of the patient's muscles at rest; postexercise recovery was less responsive to the increased dose; and a higher dose of vitamin K3 (80 mg/day) did not produce side effects. The differential therapeutic effects of vitamin K3 at rest and during exercise recovery are probably due to the differential kinetics of each metabolic state. Monitoring muscle bioenergetics with 31P-NMR is valuable in documenting therapeutic improvements in mitochondrial myopathies.

Adult↗
PubMed2005

Preparation and characterization of a copper based Indian traditional drug: tamra bhasma.

The copper based Indian traditional drug 'tamra bhasma' is administered for various ailments since long. Its synthesis involves treating metallic copper with plant juices and then repeated calcination in presence of air so that the metallic state is transformed into the corresponding oxide form traditionally known as 'bhasma'. In this work, we present a systematic characterization of this traditional drug using various techniques like X-ray diffraction (XRD), scanning electron microscopy (SEM)-energy dispersive X-ray analysis (EDX), X-ray photoelectron spectroscopy (XPS), infrared spectroscopy (IR), thermogravimetry (TG) and surface area measurement. The results obtained were found to match very well with those of a standard copper oxide confirming the composition of the drug sample. In addition, some specific findings were also made which could help in interpreting the therapeutic properties of the traditional drug 'tamra bhasma'.

Ascorbic Acid↗