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PubMed2003

Vitamin C and vitamin E restore the resistance of GSH-depleted lens cells to H2O2.

A decline in reduced glutathione (GSH) levels is associated with aging and many age-related diseases. The objective of this study was to determine whether other antioxidants can compensate for GSH depletion in protection against oxidative insults. Rabbit lens epithelial cells were depleted of > 75% of intracellular GSH by 25-200 microM buthionine sulfoximine (BSO). Depletion of GSH by BSO alone had little direct effect on cell viability, but resulted in an approximately 30-fold increase in susceptibility to H(2)O(2)-induced cell death. Experimentally enhanced levels of nonprotein sulfhydryls other than GSH (i.e., N-acetylcysteine) did not protect GSH-depleted cells from H(2)O(2)-induced cell death. In contrast, pretreatment of cells with vitamin C (25-50 microM) or vitamin E (5-40 microM), restored the resistance of GSH-depleted cells to H(2)O(2). However, concentrations of vitamin C > 400 microM and vitamin E > 80 microM enhanced the toxic effect of H(2)O(2). Although levels of GSH actually decreased by 10-20% in cells supplemented with vitamin C or vitamin E, the protective effects of vitamin C and vitamin E on BSO-treated cells were associated with significant ( approximately 70%) decreases in oxidized glutathione (GSSG) and concomitant restoration of the cellular redox status (as indicated by GSH:GSSG ratio) to levels detected in cells not treated with BSO. These results demonstrate a role for vitamin C and vitamin E in maintaining glutathione in its reduced form. The ability of vitamin C and vitamin E in compensations for GSH depletion to protect against H(2)O(2)-induced cell death suggests that GSH, vitamin C, and vitamin E have common targets in their actions against oxidative damage, and supports the preventive or therapeutic use of vitamin C and E to combat age- and pathology-associated declines in GSH. Moreover, levels of these nutrients must be optimized to achieve the maximal benefit.

Animals↗

PubMed1982

The chemically injured eye.

Chemical injury of the eye may occur in a wide range of circumstances. Of first importance is the recognition of the nature of the injury since an increasing number of toxic substances is being used in home and industry and each type of compound may produce unusual corneal and conjunctival changes. Early assessment of the severity of the corneal burn helps determine prognosis and directs treatment. The use of topical sodium ascorbate and citrate has added new prospects of reduced corneal damage while enzyme inhibitors have shown some value in preventing and controlling corneal melting. The later problems of recurrent or persistent epithelial defects require careful manipulation of the tear film and corneal environment including the use of therapeutic soft contact lenses. In the long term, attention to the whole corneal environment, especially lids, conjunctiva, and tears, becomes most important especially in selection of patients for keratoplasty and in management of the complications which may follow surgery.

Alkalies↗

PubMed1978

[Gardner's syndrome in familial popyposis: clinical contribution and etiopathogenetic, therapeutic and prognostic considerations].

Starting from one case of Gardner's syndrome of their own observation, and in light of Watne's results, the authors argue that in the syndrome just named--and in familial polyposis in a broader sense--genetic factors do not play a predominant role; rather, polyps seem to result from the prolonged action of noxious agents. At any rate, said action can be neutralized, and possibly prevented either with a surgical modification of the distal gut or by treatment with a chemical substance identified as ascorbic acid. In view of these considerations, the authors recommend preventive medical therapy.

Female↗

PubMed2003

Interplay between high energy impulse noise (blast) and antioxidants in the lung.

High-energy impulse noise (BLAST) is a physical event characterized by an abrupt rise in atmospheric pressure above ambient lasting for a very short period, but potentially causing significant material and biological damage. Exposure to high-level BLAST can be destructive and lethal. Low-level BLAST similar to what is encountered repeatedly by military personnel during training and combat from detonation of munitions and firing of large caliber weapons, and during occupational use of explosives and some heavy machinery, can also cause significant injury. Globally, civilians are increasingly exposed to BLAST resulting from terrorist bombings or abandoned unmarked mines following numerous wars and conflicts. We have shown previously in several animal models that exposure to non-lethal BLAST results in pathological changes, mostly to the hollow organs characterized in the lungs, the most sensitive organ, by rupture of alveolar septa, and pulmonary hemorrhage and edema. These events potentially can cause alveolar flooding, respiratory insufficiency and adult respiratory distress syndrome (ARDS), leading to varying degrees of hypoxia, antioxidant depletion and oxidative damage. We have also observed progressive formation of nitric oxide in blood and other tissues. The totality of these observations supports our general hypothesis that exposure to BLAST can lead to antioxidant depletion and oxidative damage. Understanding the mechanism(s) of BLAST-induced oxidative stress may have important implications that include a potential beneficial role for antioxidants as a prophylaxis or as secondary treatment of injury after exposure alongside other protective and therapeutic modalities. In addition, it suggests a role for endogenous nitric oxide in the injury. This report reviews experimental evidence of BLAST-induced antioxidant depletion, and the potential benefit from antioxidant supplementation before exposure.

Animals↗

PubMed2000

New and emerging treatments for photoaging.

It is easy to become too busy treating the sequelae of photoaging, actinic keratoses, and skin cancers to discuss prevention adequately with patients. With children, sun-protective measures and sunscreen information should be the main therapeutic intervention. In any young adult with an actinic keratosis or skin cancer, topical and resurfacing treatments should be considered. In older patients with fragile skin and solar purpura, reversal of photodamage can have a positive effect on daily functioning.

Adult↗

PubMed2004

Fenretinide induces sustained-activation of JNK/p38 MAPK and apoptosis in a reactive oxygen species-dependent manner in neuroblastoma cells.

Fenretinide, which mediates apoptosis in neuroblastoma cells, is being considered as a novel therapeutic for neuroblastoma. The cytotoxic mechanisms of fenretinide, however, have not been fully elucidated. Sustained-activation of JNK and p38 MAPK signaling has been shown recently to have a pivotal role in stress-induced apoptosis. Whether fenretinide activates the signaling in neuroblastoma cells is not known. In the present study, fenretinide induced sustained-activation of both JNK and p38 MAPK in neuroblastoma cells. Pretreatment with the antioxidant L-ascorbic acid almost completely inhibited the accumulation of fenretinide-induced intracellular reactive oxygen species (ROS), activation of JNK and p38 MAPK and apoptosis. Intracellular ROS production and activation of stress signaling was not altered by fenretinide in resistant neuroblastoma cells. Our study demonstrates that in neuroblastoma cells, fenretinide induces sustained-activation of JNK and p38 MAPK in an ROS-dependent manner and indicates that JNK and p38 MAPK signaling might mediate fenretinide-induced apoptosis. Our results also indicate that suppression of the fenretinide-induced ROS productive system and the downstream JNK and p38 MAPK signaling pathways causes neuroblastoma cells to become resistant to fenretinide.

Antineoplastic Agents↗

PubMed1990

Ferric ion-induced lipid peroxidation in erythrocyte membranes: effects of phytic acid and butylated hydroxytoluene.

Ferric ion was found to stimulate the peroxidation of erythrocyte membrane lipids, causing a biphasic and concentration-dependent increase in the formation of thiobarbituric acid reactive substances. Ascorbic acid and reduced glutathione were able to enhance this lipid peroxidation, presumably by facilitating the reduction of ferric ion. Iron chelators, such as phytic acid, ethylenediaminetetraacetic acid and uric acid, and the chain-reaction-terminating antioxidant butylated hydroxytoluene suppressed the ferric ion-induced peroxidation by actions not likely related to hydroxyl radical scavenging. The effectiveness of phytic acid, a naturally occurring antioxidant, in the inhibition of iron-dependent lipid peroxidation suggests its possible therapeutic application as a non-toxic iron chelator for ameliorating the extent of oxy-radical-induced tissue damage.

Butylated Hydroxytoluene↗

PubMed1977

Severe generalized glutathione reductase deficiency after antitumor chemotherapy with BCNU" [1,3-bis(chloroethyl)-1-nitrosourea].

Patients receiving BCNU [1,3-bis(2 chloroethyl)-1-nitrosourea] acquire a profound deficiency of erythrocytic oxidized glutathione reductase (GSSG-R) within minutes after the first intravenous injection of a single therapeutic dose (75 mg/M.2) of the drug. This effect is not accompanied by changes in the activites of 19 additional erythrocytic enzymes tested, is reproducible in vitro in a dose-related manner, and is not caused by the antitumor agents administered concurrently with the nitrosourea. The inactivation of erythrocytic GSSG-R results in decreased levels of reduced glutathione (GSH), marked GSH instability and disturbed hydrogen peroxide removal with a positibe ascorbate cyanide test and leads to increased susceptibility to oxidative hemolysis, particularly in glucose-6-phosphate dehydrogenase (G-6-D)-deficient patients. BCNU inhibits GSSG-R irreversibly, probably through alkylation rather than carbamylation, and the reappearance of enzyme activity in vivo after each chemotherapy pulse depends on the capacity of the marrow to release erythrocytes with normal activity formed during the drug-free interval. BCNU inhibits GSSG-R not only in erythrocytes but also in human leukocytes and platelets, as well as in yeast, monkey erythrocytes, and all the organs tested in the mouse. This generalized, severe, and specific GSSG-R deficiency caused by therapeutic doses of BCNU may enhance or mediate the toxic and antitumor effects of the nitrosourea and provides a simple yet sensitive biochemical means of monitoring bone marrow reserve in patients receiving multiple courses of chemotherapy with this agent.

Animals↗

PubMedDate not supplied

[Therapeutic and preventive diet and various indicators of health and work capacity of workers at the industrial plant "Sintez"].

Anthropometric investigations conducted have shown that 28.1% of the workers have excessive body mass. At the same time energy expenditure of workers at some departments and bays is within the range of 164 +/- 1.6-188.89 +/- 3.5 kcal/h. Natural resistance parameters (lysozyme activity, virus persistence) in the workers of the enterprise were lower than in the control group. Physical working capacity of 15% of the workers was rather low. Optimal providing of the body with ascorbic acid, thiamine and riboflavin was recorded only in 30-40% of the examined workers. Ration N 5 that was given to the workers was characterized by excessive energy value, low content of animal protein and vegetable fat deficiency; the content of simple sugars was 2-fold higher than the value recommended. The components of the ration are not sufficiently balanced, it does not meet the physiological needs of the workers.

Adult↗

PubMed1977

Aqueous humor ascorbate concentration and open-angle glaucoma.

The mean value for aqueous concentration in 35 patients with open-angle glaucoma was 22.4 +/- 12.9 mg/100 ml. The mean value for aqueous ascorbate in four patients with uncomplicated senile cataract was 11.55 +/- 3.01 mg/100 ml. The results indicate that the majority of open-angle glaucomatous eyes do not involve a deficiency of ascorbate, and suggest that ascorbate has no therapeutic value in the management of primary open-angle glaucoma. The magnitude of aqueous ascorbate variation among glaucoma eyes is probably related to the factors that influence the patency of trabecular meshwork, not the metabolic activity of the ciliary processes.

Animals↗

PubMedDate not supplied

Diabetes mellitus is controlled by vitamin C treatment.

The present study was started to investigate the question of whether or not vitamin C administration may help control diabetes mellitus (DM) by stimulating the insulin mechanism of a DM patient. We were motivated to take up the above thesis by the anticipation that vitamin C, being detectable in abundance in endocrine cells, may play a cardinal role in the production of hormones. In the preliminary experiment, we investigated the relation between glucose, insulin and vitamin C in the plasma of a non-diabetic male volunteer in whom vitamin C was introduced intravenously either by injection or by infusion, and with or without concomitant administration of glucose. In the follow-up study of 3 DM patients, the effect of the vitamin C infusion therapy on DM was assessed by summing up multiple clinical information. Results obtained are as follows: 1) the drip infusion system was superior to the ordinary injection system for maintaining plasma concentration of vitamin C at a high level and for a long period. 2) The plasma concentration of insulin, when tested in the vitamin C infusion system, followed a bimodal curve--a finding to suggest that vitamin C may stimulate the insulin mechanism in 2 distinct ways. The early mode was glucose-dependent at its height, but the late mode was independent of glucose charge. 3) The praxis of vitamin C infusion produced clinical improvements in 3 DM patients. The therapeutic efficacy of the treatment varied from patient to patient. In all cases, control of DM was started by combined use of the vitamin C infusion treatment and the insulin injection treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗

PubMed2006

Polymeric systems for amorphous Delta9-tetrahydrocannabinol produced by a hot-melt method. Part II: Effect of oxidation mechanisms and chemical interactions on stability.

The objectives of the present research investigations were to (i) elucidate the mechanism for the oxidative degradation of Delta(9)-tetrahydrocannabinol (THC) in polymer matrix systems prepared by a hot-melt fabrication procedure, and (ii) study the potential for controlling these mechanisms to reduce the degradation of THC in solid dosage formulations. Various factors considered and applied included drug-excipient compatibility, use of antioxidants, cross-linking in polymeric matrices, microenvironment pH, and moisture effect. Instability of THC in polyethylene oxide (PEO)-vitamin E succinate (VES) patches was determined to be due to chemical interaction between the drug and the vitamin as well as with the atmospheric oxygen. Of the different classes and mechanisms of antioxidants studied, quenching of oxygen by reducing agents, namely, ascorbic acid was the most effective in stabilizing THC in PEO-VES matrices. Only 5.8% of the drug degraded in the ascorbic acid-containing patch as compared to the control (31.6%) after 2 months of storage at 40 degrees C. This coupled with the cross-linking extent and adjustment of the pH microenvironment, which seemed to have an impact on the THC degradation, might be effectively utilized towards stabilization of the drug in these polymeric matrices and other pharmaceutical dosage forms. These studies are relevant to the development of a stable transmucosal matrix system for the therapeutic delivery of amorphous THC.

Antioxidants↗

PubMed1998

Rhenium-186-mercaptoacetyltriglycine-labeled monoclonal antibody for radioimmunotherapy: in vitro assessment, in vivo kinetics and dosimetry in tumor-bearing nude mice.

Stability and immunoreactivity of 186Re-labeled monoclonal antibody were examined, and its in vivo kinetics was investigated in tumor-bearing Balb/c nu/nu female mice to assess the feasibility of using it in radioimmunotherapy (RIT). A murine IgG1, A7, against a 45 kD glycoprotein in human colon cancer was radiolabeled with 186Re by using a chelating method with a mercaptoacetyltriglycine (MAG3). 186Re-MAG3 complex was conjugated to A7 after esterification of 186Re-MAG3 with tetrafluorophenol (TFP). The efficiency of 186Re-MAG3-TFP production and the labeling efficiency of A7 were 51-59% and 57-60%, respectively. Immunoreactivity of purified 186Re-MAG3-A7 was 68.2% at infinite antigen excess. In 0.9% NaCl at 4 degrees C, the radioactivity (12.7 MBq/mg, 3.55 MBq/ml) dissociated with time from 186Re-MAG3-A7 as a small molecular weight moiety because of autoradiolysis. The addition of ascorbic acid, 5 mg/ml, as a radioprotectant or storage at -80 degrees C could effectively prevent the radiolysis of 186Re-MAG3-A7 for 7 days. Immunoreactivity of 186Re-MAG3-A7, 6.70 MBq/mg (6.66 MBq/ml), stored in the presence of ascorbic acid was well retained up to 8 days after the preparation. In colon cancer xenografted mice, 31.0% of the injected dose/g of 186Re-MAG3-A7 had accumulated in the tumors at 24 h postinjection. Estimated radiation dose to tumors was 14.9 cGy/37 kBq up to 8 days postinjection which was 12-fold greater than the whole-body radiation dose. These in vivo characteristics were superior to those of A7 labeled with radioiodine, affording greater therapeutic ratios than 131I-A7. Because of the better image quality of 186Re-MAG3-A7 as well as more favorable dosimetry, 186Re-MAG3-A7 would be a better choice for RIT of colon cancer than 131I-A7. These results indicated the feasibility of RIT with 186Re-MAG3-A7, though the prevention of radiolysis of the labeled antibody should be considered.

Animals↗

PubMed1972

The influence of drugs upon the anticoagulant activity of heparin.

Although physical incompatibility between heparin and a number of drugs has been reported we did not discover any evidence of such incompatibility when heparin was mixed with 11 commonly used drugs in therapeutic concentrations.Furthermore, there was no detectable change in the anticoagulant activity in the presence of any of these drugs, nor was there any change in the biological activity of the antibiotics tested.

Ampicillin↗

PubMed2006

Historic and current strategies in bone tissue engineering: do we have a hope in Hench?

Professors Larry Hench and Julia Polak formed the Tissue Engineering and Regenerative Medicine Centre (TERM) at Imperial College London to foster collaborations between biologists and materials scientists. Early work at the center elucidated the biomolecular interactions between primary human osteoblasts and 45S5 Bioglass . As research efforts expanded, the team discovered that the dissolution products of both 45S5 Bioglass and 58S sol-gel bioactive glasses had osteoblastic stimulatory properties. To address the shortage of appropriate cells for bone tissue engineering applications, TERM scientists also demonstrated the differentiation of embryonic stem (ES) cells to osteoblasts when treated with the dissolution products of bioactive glasses. They also found that the soluble factors ascorbic acid, beta -glycerophosphate, and dexamethasone preferentially differentiated ES cells to osteoblasts, and their combination with the dissolution products of bioactive glasses stimulated differentiation even further. Taken together, these results demonstrate the suitability of bioactive glasses as scaffolds for bone tissue engineering as they not only provide an osteoconductive and osteoproductive substrate, but also actively stimulate cells to express appropriate osteoblastic phenotypes. Professor Hench's vision to pioneer regenerative medicine research continues with the aim of developing novel therapeutics to treat musculoskeletal disability.

Animals↗

PubMed2001

An analog of the human albumin N-terminus (Asp-Ala-His-Lys) prevents formation of copper-induced reactive oxygen species.

Copper mobilization and redox activity form damaging reactive oxygen species (ROS) and are implicated in the pathogenesis of ischemia-reperfusion injury, chronic inflammation, Alzheimer's disease, aging, and cancer. Protein sequestration of Cu(II) ions has been shown to prevent ROS-generating reactions. The first four amino acids of the N-terminus of human albumin, Asp-Ala-His-Lys (DAHK), form a tight binding site for Cu(II) ions. We synthesized several analogs, including the enantiomer d-DAHK, to study their effects on copper-induced hydroxyl radical and superoxide formation in the presence of ascorbate. d-DAHK prevented thiobarbituric acid-reactive species (TBARS) formation within physiological and acidic pH ranges (7.5-6.5) and inhibited low-density lipoprotein lipid peroxidation. A d-DAHK/Cu complex exhibited superoxide dismutase-like activity by significantly inhibiting superoxide formation. These in vitro results suggest that d-DAHK may shift the Cu(II)-binding equilibrium from the exchangeable Cu(II) pool to the tightly-bound, nonexchangeable pool, prevent ROS formation, and potentially provide therapeutic benefit for ROS-related diseases.

Albumins↗

PubMed1978

[Proliferation of L 929 mouse fibroblasts and synthesis of active peptidyl prolyl hydroxylase in these cells in monolayer culture under the influence of D-penicillamine, azathioprine, aurothiopolypeptide, oxyphenbutazone and prednisolone (author's transl)].

L 929 mouse fibroblasts were cultured as monolayer using MEM Eagle medium after addition of bovine serum albumin, antibiotics, antimycotica, ferrous nitrate and ascorbic acid. In 24 hours distances cell number was counted. At the same time peptidyl prolyl hydroxylase activity was determined and related to the protein concentration in the cells. The proliferation of the cells followed a typical curve. The cell number decreased after trypsination, then increased logarithmically, finally reached a stationary phase. Enzyme activity showed a correspondent curve. Active enzyme did not appear until near the end of the log phase. After addition of the mesenchyme active substances in therapeutical concentrations proliferation and synthesis of active peptidyl prolyl hydroxylase in the cells were significantly decreased. The results are discussed in relation to the characteristics of collagen synthesis and proliferation of connective tissue cells under physiological, pathophysiological and therapeutical conditions.

Animals↗

PubMed1993

Antimutagenic efficacy of higher doses of vitamin C.

Vitamin C, when administered concurrently with a pesticide (endosulfan, phosphamidon or mancozeb), could significantly decrease the frequency of pesticide-induced clastogenic and mitosis-disruptive changes in the bone marrow cells of young Swiss albino mice. Of the three doses (10, 20 or 40 mg/kg b.wt./day) of the vitamin, the one which is double the human therapeutic dose (20 mg/kg b.wt./day) was most effective as an antimutagen to be followed by 40 mg and 10 mg. None of these doses of vitamin C showed any genotoxicity of their own for the parameters studied here.

Animals↗