Taken together, these data indicate that ascorbate at concentrations achieved
only by i.v. administration may be a pro-drug for formation of H2O2, and that blood can be a delivery system of the pro-drug to tissues.
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Refurbished Alaris Signature 7130 Infusion IV Pump - 0 views
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Refurbished Alaris Signature 7130 Infusion IV Pump The Alaris IVAC Signature Gold 7130 Infusion Pump is a single channel volumetric infusion pump that allows independent programming on both sides. It can be used for general IV infusions, antibiotics, blood infusions, enteral infusions, TPN and hyperalimentation, and lipids. Dual-rate piggyback function and panel lock.
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Refurbished Alaris Signature 7130 Infusion IV Pump - 0 views
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Refurbished Alaris Signature 7130 Infusion IV Pump The Alaris IVAC Signature Gold 7130 Infusion Pump is a single channel volumetric infusion pump that allows independent programming on both sides. It can be used for general IV infusions, antibiotics, blood infusions, enteral infusions, TPN and hyperalimentation, and lipids. Dual-rate piggyback function and panel lock.
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Refurbished Baxter Sigma Spectrum Infusion IV Pump - 0 views
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The Baxter SIGMA Spectrum Infusion System is redefining smart technology with Second Generation software to help prevent pump-related medication errors.
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The Baxter SIGMA Spectrum Infusion System is redefining smart technology with Second Generation software to help prevent pump-related medication errors.
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Refurbished LifeCare Abbott Hospira Plum 5000 Infusion IV Pump is a single channel volumetric infusion pump with data port for external communications. It is a multi-line, general purpose infusion system designed to meet the need for hospital-wide device standardization. * Refurbished * 1-Year Warranty .
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Refurbished Baxter Sigma Spectrum Infusion IV Pump - 0 views
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The Baxter SIGMA Spectrum Infusion System is redefining smart technology with Second Generation software to help prevent pump-related medication errors. The SIGMA Spectrum Infusion System provides multiple error prevention systems along with bi-directional wireless communication and comprehensive log analysis software to create CQI reports. SIGMA Spectrum pump provides rapid, intuitive work-flow using a bright, easy to read color display and on-board digital help screens.
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The Baxter SIGMA Spectrum Infusion System is redefining smart technology with Second Generation software to help prevent pump-related medication errors. The SIGMA Spectrum Infusion System provides multiple error prevention systems along with bi-directional wireless communication and comprehensive log analysis software to create CQI reports. SIGMA Spectrum pump provides rapid, intuitive work-flow using a bright, easy to read color display and on-board digital help screens. SIGMA Spectrum pump also provides economic value by utilizing Baxter's standard IV administration sets.
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Pharmacologic ascorbic acid concentrations selectively kill cancer cells: Action as a p... - 0 views
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IV vitamin C cancer ascorbic acid vitamin C H2O2 GPX glutathione Perioxidase
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These findings give plausibility to i.v. ascorbic acid in cancer treatment, and have unexpected implications for treatment of infections where H2O2 may be beneficial
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pharmacologic concentrations of ascorbate killed cancer but not normal cells, that cell death was dependent only on extracellular but not intracellular ascorbate, and that killing was dependent on extracellular hydrogen peroxide (H2O2) formation with ascorbate radical as an intermediate
- ...48 more annotations...
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Our data show that ascorbic acid selectively killed cancer but not normal cells, using concentrations that could only be achieved by i.v. administration
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Ascorbate-mediated cell death was due to protein-dependent extracellular H2O2 generation, via ascorbate radical formation from ascorbate as the electron donor. Like glucose, when ascorbate is infused i.v., the resulting pharmacologic concentrations should distribute rapidly in the extracellular water space (42). We showed that such pharmacologic ascorbate concentrations in media, as a surrogate for extracellular fluid, generated ascorbate radical and H2O2. In contrast, the same pharmacologic ascorbate concentrations in whole blood generated little detectable ascorbate radical and no detectable H2O2. These findings can be accounted for by efficient and redundant H2O2 catabolic pathways in whole blood (e.g., catalase and glutathione peroxidase) relative to those in media or extracellular fluid
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ascorbic acid administered i.v. in pharmacologic concentrations may serve as a pro-drug for H2O2 delivery to the extracellular milieu
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H2O2 generated in blood is normally removed by catalase and glutathione peroxidase within red blood cells, with internal glutathione providing reducing equivalents
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The electron source for glutathione is NADPH from the pentose shunt, via glucose-6-phosphate dehydrogenase. If activity of this enzyme is diminished, the predicted outcome is impaired H2O2 removal causing intravascular hemolysis, the observed clinical finding.
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Only recently has it been understood that the discordant clinical findings can be explained by previously unrecognized fundamental pharmacokinetics properties of ascorbate
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Intracellular transport of ascorbate is tightly controlled in relation to extracellular concentration
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Intravenous ascorbate infusion is expected to drastically change extracellular but not intracellular concentrations
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For i.v. ascorbate to be clinically useful in killing cancer cells, pharmacologic but not physiologic extracellular concentrations should be effective, independent of intracellular ascorbate concentrations.
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There was no correlation with ascorbate-induced cell death and glutathione, catalase activity, or glutathione peroxidase activity.
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H2O2, as the product of pharmacologic ascorbate concentrations, has potential therapeutic uses in addition to cancer treatment, especially in infections
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Use of ascorbate as an H2O2-delivery system against sensitive pathogens, viral or bacterial, has substantial clinical implications that deserve rapid exploration.
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Recent pharmacokinetics studies in men and women show that 10 g of ascorbate given i.v. is expected to produce plasma concentrations of nearly 6 mM, which are >25-fold higher than those concentrations from the same oral dose
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As much as a 70-fold difference in plasma concentrations is expected between oral and i.v. administration,
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Complementary and alternative medicine practitioners worldwide currently use ascorbate i.v. in some patients, in part because there is no apparent harm
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We first investigated whether ascorbate in pharmacologic concentrations selectively affected the survival of cancer cells by studying nine cancer cell lines
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Clinical pharmacokinetics analyses show that pharmacologic concentrations of plasma ascorbate, from 0.3 to 15 mM, are achievable only from i.v. administration
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plasma ascorbate concentrations from maximum possible oral doses cannot exceed 0.22 mM because of limited intestinal absorption
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For five of the nine cancer cell lines, ascorbate concentrations causing a 50% decrease in cell survival (EC50 values) were less than 5 mM, a concentration easily achievable from i.v. infusion
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All tested normal cells were insensitive to 20 mM ascorbate.
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As ascorbate concentration increased, the pattern of death changed from apoptosis to pyknosis/necrosis, a pattern suggestive of H2O2-mediated cell death
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Apoptosis occurred by 6 h after exposure, and cell death by pyknosis was ≈90% at 14 h after exposure
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In contrast to lymphoma cells, there was little or no killing of normal lymphocytes and monocytes by ascorbate
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Ascorbate is transported into cells as such by sodium-dependent transporters, whereas dehydroascorbic acid is transported into cells by glucose transporters and then immediately reduced internally to ascorbate
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Whether or not intracellular ascorbate was preloaded, extracellular ascorbate induced the same amount and type of death.
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extracellular ascorbate in pharmacologic concentrations mediates death of lymphoma cells by apoptosis and pyknosis/necrosis, independently of intracellular ascorbate.
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Because these data implicated H2O2 in cell killing, we added H2O2 to lymphoma cells and studied death patterns using nuclear staining (19, 28). The death patterns found with exogenous H2O2 exposure were similar to those found with ascorbate
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For both ascorbate and H2O2, death changed from apoptosis to pyknosis/necrosis as concentrations increased
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Sensitivity to direct exposure to H2O2 was greater in lymphoma cells compared with normal lymphocytes and normal monocytes
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There was no association between the EC50 for ascorbate-mediated cell death and intracellular glutathione concentrations, catalase activity, or glutathione peroxidase activity
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H2O2 generation was dependent on time, ascorbate concentration, and the presence of trace amounts of serum in media
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whatever H2O2 is generated should be removed by glutathione peroxidase and catalase within red blood cells, because H2O2 is membrane permeable
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The data are consistent with the hypothesis that ascorbate in pharmacologic concentrations is a pro-drug for H2O2 generation in the extracellular milieu but not in blood.
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In patients with glucose-6-phosphate dehydrogenase deficiency, i.v. ascorbate is contraindicated because it causes intravascular hemolysis
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ascorbate, an electron-donor in such reactions, ironically initiates pro-oxidant chemistry and H2O2 formation
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data here showed that ascorbate initiated H2O2 formation extracellularly, but H2O2 targets could be either intracellular or extracellular, because H2O2 is membrane permeant
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More than 100 patients have been described, presumably without glucose-6-phosphate dehydrogenase deficiency, who received 10 g or more of i.v. ascorbate with no reported adverse effects other than tumor lysis
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Intravenous Ascorbate as a Tumor Cytotoxic Chemotherapeutic Agent - 0 views
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Ascorbic acid and its salts (AA) are preferentially toxic to tumor cells in vitro (6 — 13) and in vivo
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Increases animal and human resistance to infectious agents by enhancing lymphocyte blastogenesis, enhancing cellular immunity, strengthening the extracellular matrix, and enhancing bactericidal activity of neutrophils and modulation of complement protein
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Strengthens the structural integrity of the extracellular matrix which is responsible for stromal resistance to malignant invasiveness
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In 1977, Bram et al reported preferential AA toxicity for several malignant melanoma cell lines, including four human-derived lines
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Noto et al reported that AA plus vitamin K3 had growth inhibiting action against three human tumor cell lines at non-toxic levels
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The AA begins to reduce cell proliferation in the tumor cell line at the lowest concentration, 1.76 mg/dl, and is completely cytotoxic to the cells at 7.04 mg/dl
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preferential toxicity of AA for tumor cells. >95% toxicity to human endometrial adenocarcinoma and pancreatic tumor cells (ATCC AN3-CA and MIA PaCa-2) occurred at 20 and 30 mg/dl, respectively.
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No toxicity or inhibition was demonstrated in the normal, human skin fibroblasts (ATCC CCD 25SK) even at the highest concentration of 50 mg/dl.
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Cameron and Pauling have published extensive suggestive evidence for prolonged life in terminal cancer patients orally supplemented (with and without initial intravenous AA therapy) with 10 g/day of AA
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the long-term, oral dosage used in those experiments (10 g/day), while substantial and capable of producing immunostimulatory and extracellular matrix modulation effects, was not high enough to achieve plasma concentrations that are generally cytotoxic to tumor cells in culture
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5 — 40 mg/dl of AA is required in vitro to kill 100% of tumor cells within 3 days. The 100% kill levels of 30 mg/dl for the endometrial carcinoma cells and 40 mg/dl for the pancreatic carcinoma cells in Figure 2 are typical
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1 h after beginning his first 8-h infusion of 115 g AA (Merit Pharmaceuticals, Los Angeles, CA), the plasma AA was 3.7 mg/dl and at 5 h was 19 mg/dl. During his fourth 8-h infusion, 8 days later, the 1 h plasma level was 158 mg/dl and 5 h was 185 mg/dl
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plasma levels of over 100 mg/dl have been maintained in 3 patients for more than 5 h using continuous intravenous infusion
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In rare instances of patients with widely disseminated and rapidly proliferating tumors, intravenous AA administration (10 — 45 g/day) precipitated widespread tumor hemorrhage and necrosis, resulting in death
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Although the outcomes were disastrous in these cases, they are similar to the description of tumor-necrosis-factor-induced hemorrhage and necrosis in mice (52) and seem to demonstrate the ability of AA to kill tumor cells in vivo.
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toxic effects of AA on one normal cell line were observed at 58.36 mg/dl and the lack of side effects in patients maintaining >100 mg/dl plasma levels
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Although it is very rare, tumor necrosis, hemorrhage, and subsequent death should be the highest priority concern for the safety of intravenous AA for cancer patients.
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Cathcart (55) who describes no ill effects with doses of up to 200 g/d in patients with various pathological conditions
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following circumstances: renal insufficiency, chronic hemodialysis patients, unusual forms of iron overload, and oxalate stone formers
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Screening for red cell glucose-6-phosphate dehydrogenase deficiency, which can give rise to hemolysis of red blood cells under oxidative stress (57), should also be performed
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any cancer therapy should be started at a low dosage to ensure that tumor hemorrhage does not occur.
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a scorbutic rebound effect can be avoided with oral supplementation. Because of the possibility of a rebound effect, measurement of plasma levels during the periods between infusions should be performed to ensure that no such effect takes place
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Every effort should be made to monitor plasma AA levels when a patient discontinues intravenous AA therapy.
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