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At least 217 records · Page 12Linked to original sources
PubMed2005

Modulation of N-methyl-N-nitrosourea induced mammary tumors in Sprague-Dawley rats by combination of lysine, proline, arginine, ascorbic acid and green tea extract.

INTRODUCTION: The limited ability of current treatments to control metastasis and the proposed antitumor properties of specific nutrients prompted us to examine the effect of a specific formulation (nutrient supplement [NS]) of lysine, proline, arginine, ascorbic acid, and green tea extract in vivo on the development of N-methyl-N-nitrosourea (MNU)-induced mammary tumors in rats. METHODS: A single intraperitoneal dose of MNU was injected into each of 20 female Sprague-Dawley rats (aged 50 days) to induce tumors. Two weeks after MNU treatment, a time by which the animals had recovered from MNU-induced toxicity, the rats were divided into two groups. Rats in group 1 (n = 10) were fed Purina chow diet, whereas those in group 2 (n = 10) were fed the same diet supplemented with 0.5% NS. After a further 24 weeks, the rats were killed and tumors were excised and processed. RESULTS: NS reduced the incidence of MNU-induced mammary tumors and the number of tumors by 68.4%, and the tumor burden by 60.5%. The inhibitory effect of NS was also reflected by decreased tumor weight; the tumor weights per rat and per group were decreased by 41% and 78%, respectively. In addition, 30% of the control rats developed ulcerated tumors, in contrast to 10% in the nutrient supplemented rats. CONCLUSION: These findings suggest that the specific formulation of lysine, proline, arginine, ascorbic acid, and green tea extract tested significantly reduces the incidence and growth of MNU-induced mammary tumors, and therefore has strong potential as a useful therapeutic regimen for inhibiting breast cancer development.

Alkylating Agents↗
PubMed1987

Heterologous immunoprecipitates also have potential for therapeutic use.

Potential therapeutic usefulness of administered enzymes is limited by toxicity and allergenicity. To overcome these problems we are using scurvy to test various enzyme modifications that may be suitable for therapy. L-Gulonolactone oxidase, which catalyzes the final step in ascorbic acid biosynthesis, is immunoprecipitated with specific antisera from rabbits and then cross-linked with glutaraldehyde. The modified enzyme retains activity sufficient to elicit ascorbic acid synthesis in scorbutic guinea pigs. Intraperitoneal injection of this altered enzyme to animals supplemented with L-gulonolactone increases plasma concentrations of the vitamin. Importantly, multiple doses of the complex are tolerated. Therefore, it is possible to prolong survival time of animals fed an ascorbic acid-deficient diet by this enzyme replacement therapy. This procedure can also be applied to other enzymes that have potential therapeutic use. Serum cholinesterase and asparaginase both retain activity after this modification and are tolerated in single or in weekly repeated injections. Following three or four weekly injections, an anaphylactic reaction to serum but not to enzyme can be elicited if they are injected intravascularly. We conclude that the stability of the immobilized foreign enzyme is a critical factor in lessening the toxicity to multiple injections of these foreign proteins.

Animals↗
PubMed1986

Preventive effect of vitamin C (L-ascorbic acid) on methylcholanthrene-induced soft tissue sarcomas in mice.

The effect of vitamin C (L-ascorbic acid) on methylcholanthrene (MCA)-induced local malignant sarcomas in mice was investigated. Four groups of mice were given single intramuscular application of MCA at a dose level of 0.5 mg/0.1 ml olive oil for each animal. Doses of 6, 25, and 35 mg vitamin C (VC)/mouse were given to animals of groups B, C and D, respectively. VC was applied in drinking water by intragastric administration 5 times weekly for the first 20 weeks. Animals of group A served as carcinogenic controls. The application of VC statistically prevented the induction of sarcomas in mice of groups B, C and D compared to carcinogenic controls (group A). VC supplementation did not significantly reduce the diameters and weights of tumors. It was concluded that, under the experimental conditions conducted, VC significantly prevented the induction of sarcomas in mice providing a good prophylactic activity; however, it did not achieve a significant therapeutic level.

Administration, Oral↗
PubMed1998

Comparison of topical therapy for striae alba (20% glycolic acid/0.05% tretinoin versus 20% glycolic acid/10% L-ascorbic acid).

BACKGROUND: Topical treatment of striae rubra with 0.1% tretinoin and laser treatment of striae rubra and alba with the 585-nm pulsed dye laser are proven therapeutic options. However, little efficacy has been shown for treatment of striae alba topically, and the laser is currently not a suitable treatment option for darker ethnic skin types. OBJECTIVE: The purpose of this study was to demonstrate that selected commercial topical agents can improve the appearance of striae alba. METHODS: Ten patients of varying skin types (I-V) having straie distensae alba on the abdomen or thighs were selected to evaluate the effectiveness of two topical treatment regimens. Patients were placed on daily topical application of 20% glycolic acid (MD Forte) to the entire treatment area. In addition, the patients applied 10% L-ascorbic acid, 2% zinc sulfate, and 0.5% tyrosine to half to the treatment area and 0.05% tretinoin emollient cream (Renova) to the other half of the treatment area. The creams were applied on a daily basis for 12 weeks. Improvement was evaluated at 4 and 12 weeks in an objective unblinded fashion at the follow-up visits, a objective blinded fashion by visual grading at the conclusion of the study, and in an objective blinded fashion with profilometry. Additionally, histopathologic analysis was performed. RESULTS: Analysis of these data reveals: 1) both regimens can improve the appearance of stretch marks; 2) these topical therapy regimens are safe and effective in study patients with minimal irritation; 3) elastin content within the reticular and papillary dermis can increase with topical 20% glycolic acid combined with 0.05% tretinoin emollient cream therapy; 4) both regimens increased epidermal thickness and decreased papillary dermal thickness in treated stretch marks when compared with untreated stretch marks; 5) combined epidermal and papillary dermal thickness in stretch marks treated with either topical regimen approaches that of normal skin; and 6) profilometry can objectively measure differences in skin texture associated with striae treatments when compared to controls, however, it is not sensitive enough to justify comparison or quantitative improvements between similarly effective treatments.

Abdomen↗
PubMed1976

Vitamin C and acute illness in Navajo schoolchildren.

To evaluate earlier observations, including our own, showing usefulness of vitamin C for managing the common cold, we performed a double-blind trial of vitamin C versus placebo in 868 children. There was no difference in number becoming ill (133 versus 129), number of episodes (166 versus 159) or mean illness duration (5.5 versus 5.8 days) between the groups. Children receiving vitamin C had fewer throat cultures yielding beta-hemolytic streptococcus (six versus 13, P less than 0.10), but no difference in overall complicated illness rate (24 versus 25). Plasma ascorbic acid levels were higher in the vitamin group 24 to 26 hours after supplementation (1.28 versus 1.04 mg per 100 ml, P less than 0.01). Children with high plasma ascorbic acid concentrations had longer mean illness (6.8 versus 4.0 days, P less than 0.05) than those with low levels. Vitamin C does not seem to be an effective prophylactic or therapeutic agent for upper respiratory illness.

Acute Disease↗
PubMed2000

Inhibition of LDL oxidation and oxidized LDL-induced cytotoxicity by dihydropyridine calcium antagonists.

PURPOSE: The antioxidant activity of dihydropyridine calcium channel antagonists was evaluated based on LDL oxidation kinetics, oxidative cell injury associated with reactive species generation, and increases in free intracellular calcium (Ca2+) levels. Interactions with ascorbic acid were studied under conditions representative of LDL oxidation in plasma and tissue. METHODS: Analysis of antioxidant activity utilized measurements of one-electron oxidation potentials and scavenging of peroxy radical-mediated oxidation. LDL antioxidant potency was determined spectrophotometrically using copper-mediated oxidation kinetics in the absence and presence of 100 microM ascorbic acid. Prevention of oxidant-induced endothelial cell injury was determined from the formation of reactive oxygen species generation and increases in intracellular free calcium concentrations following addition of oxidized LDL or linoleic acid hydroperoxide. RESULTS: Felodipine and amlodipine effectively inhibit peroxyl radical-mediated oxidation in lipoproteins and cells that is markedly enhanced in the presence of ascorbic acid. In the presence of ascorbic acid, inhibition of LDL oxidation is over four times greater than in LDL treated without antioxidants, and oxidized LDL and linoleic acid hydroperoxide-induced reactive oxygen species formation is effectively suppressed in cells. Inhibition of intracellular calcium increases was achieved using nM concentrations of felodipine or amlodipine. CONCLUSIONS: The additive effect for ascorbic acid and the calcium channel antagonist is postulated to involve a combination of peroxide-degrading and peroxyl radical scavenging reactions, demonstrating the importance of lipid peroxides during LDL oxidation and oxidized LDL-induced cytotoxicity. Cytoprotection is associated with inhibition of oxidant-induced increases in intracellular free calcium. Both the cytoprotective and LDL antioxidant activity for these compounds is manifested at concentrations approaching the therapeutic levels found in plasma.

Animals↗
PubMed1999

Effect of topically applied 0.1% dexamethasone on endothelial healing and aqueous composition during the repair process of rabbit corneal alkali wounds.

PURPOSE: The effects of topical dexamethasone on the endothelial healing and the change of aqueous compositions were investigated during the repair process of alkali-wounded rabbit cornea. METHODS: A central corneal alkali wound was produced by a 60 sec application of a 5.5 mm round filter paper soaked in 1N NaOH onto one eye of each rabbit. The eyes subsequently were treated topically with either 0.1% dexamethasone or a balanced salt solution (BSS) 4 times per day for 8 weeks. Endothelial wound morphometry was performed after alizarin red and trypan blue staining. The concentrations of ascorbic acid, glucose, and the ions, Na+, K+, Ca2+ and Mg2+, were measured in the aqueous humor. RESULTS: Endothelial healing in control (alkali-wounded but not treated with dexamethasone) corneas showed a biphasic pattern of healing: an initial short-term healing for the first week and then a late long-term healing following the secondary endothelial breakdown. Topical administration of 0.1% dexamethasone deterred endothelial healing during the early period and prevented the secondary endothelial breakdown. However, the total repair process of endothelium was accelerated by the dexamethasone-treatment. Among the various components of the aqueous humor examined, ascorbic acid seemed the most sensitive to change caused by the alkali injury and dexamethasone treatment. CONCLUSIONS: The present data indicate that dexamethasone may have a therapeutic potential in the management of endothelial healing after corneal alkali injury.

Administration, Topical↗
PubMed1989

In vitro protection by erdosteine against oxidative inactivation of alpha-1-antitrypsin by cigarette smoke.

Direct exposure in vitro of the protein alpha 1-antitrypsin (alpha 1-AT; human neutrophil elastase inhibitor, alpha 1-proteinase inhibitor) to gas phase cigarette smoke causes a loss of elastase-inhibitory capacity (EIC). This effect appears to be related to the formation of reactive oxygen species in the smoke that inactivate alpha 1-AT by oxidizing the methionine terminal amino acid. Reducing agents such as glutathione and ascorbic acid prevent this inactivation. In the present investigation erdosteine, a novel thiol derivative, which contains two blocked SH groups with potential reducing properties, was tested in vitro for its capacity to protect human alpha 1-AT. For the purpose, the compound, previously hydrolyzed with bicarbonate-carbonate buffer or with microsomal enzymes was put in contact with alpha 1-AT and exposed to gas phase cigarette smoke. The EIC of alpha 1-AT was then measured by incubating the samples with leukocyte elastase and, subsequently, by titrating the residual elastolytic activity against a synthetic substrate. Under these conditions erdosteine effectively protected alpha 1-AT against the smoke injury and, after alkaline hydrolysis, it appeared to be as active as glutathione and ascorbic acid (EC50 being respectively 6.4, 7.2 and 6.2 mM). This evidence suggests that the erdosteine SH groups, which can become free, may have an important role in the mechanism of action, by blocking highly reactive oxygen-free radicals. Erdosteine may have a therapeutic application in preventing oxidative lung damage induced by cigarette smoke.

Ascorbic Acid↗
PubMed1987

Ascorbate potentiates DNA damage by 1-methyl-1-nitrosourea in vivo and generates DNA strand breaks in vitro.

Ascorbic acid (vitamin C) is an important intracellular reducing agent. It also has been suggested to be (i) a protective agent against development of cancer, (ii) a therapeutic agent for malignancies and (iii) a mutagen. We have found that high concentrations of ascorbate leads to DNA damage in several in vivo and in vitro situations. Guinea-pigs receiving oral 1-methyl-1-nitrosourea (MNU) were used as a whole animal model. Administration of sodium ascorbate prior to MNU increased strand breakage in pancreatic DNA. Concentrations of ascorbate greater than 0.5 mM increased the frequency of DNA strand breaks caused by MNU in both L1210 murine leukemia cells and guinea-pig pancreatic cells in tissue culture; ascorbate alone led to DNA strand breaks in the latter cells. Investigations of the mechanism of DNA damage were carried out with purified DNA. Ascorbate produced single- and double-strand breaks in plasmid DNA. Cleavage was catalyzed by copper(II), inhibited by catalase and blocked by the presence of thiols. We conclude that superoxide and hydrogen peroxide produced during the oxidation of ascorbate leads to generation of hydroxyl free radicals that can mediate DNA strand scissions and potentiate the effects of alkylating carcinogens.

Animals↗