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Vitamin C Pharmacokinetics: Implications for Oral and Intravenous Use - 0 views

www.annals.org/...533.full IV vitamin C intravenous cancer
shared by Nathan Goodyear on 14 Nov 11 - No Cached
  • Nathan Goodyear on 14 Nov 11
     
    only vitamin C IV shown to raise plasma and urine levels when compared to oral intake in cancer patients
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Antioxidants as Therapeutic Agents for Liver Disease - 0 views

www.ncbi.nlm.nih.gov/...PMC3228367 IV vitamin C IV intravenous C antioxidant therapy antioxidants hepatitis liver
shared by Nathan Goodyear on 25 Sep 13 - No Cached
  • Nathan Goodyear on 25 Sep 13
     
    This study concludes that evidence is small and inadequate despite consistent reductions of elevated liver enzymes.  The review of the data here includes both IV and oral therapy.  These modalities are not comparable.  IV vitamin C has been shown to reduce elevated liver enzymes where oral does not.
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Intravenously administered vitamin C as cancer therapy: three cases -- Padayatty et al.... - 0 views

www.cmaj.ca/...937 intravenously vitamin C cancer
shared by Nathan Goodyear on 09 Feb 11 - Cached
  • high-dose vitamin C, given by intravenous and oral routes, may improve symptoms and prolong life in patients with terminal cancer
  • Nathan Goodyear on 09 Feb 11
     
    High-dose IV vitamin C benefits cancer patients:review of 3 case studies
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Antioxidant and pro-oxidant activity of Vitamin C in oral environment Chakraborthy A, R... - 0 views

www.ijdr.in/article.asp vitamin c pro-oxidant antioxidant cancer IV vitamin c
shared by Nathan Goodyear on 11 Jul 19 - No Cached
  • Nathan Goodyear on 11 Jul 19
     
    Vitamin C has both antioxidant and pro-oxidant effects
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The antioxidant effects of vitamin C on liver enzymes: aspartate aminotransferase, alan... - 0 views

www.pagepressjournals.org/...1170 vitamin C liver enzymes antioxidant
shared by Nathan Goodyear on 18 Sep 13 - No Cached
  • Nathan Goodyear on 18 Sep 13
     
    Vitamin C, in oral route, prevents elevations in liver enzymes after liver insult from Paraquat.
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World J Gastroenterol - 0 views

www.wjgnet.com/...5317.htm hepatitis IV vitamin C IV intravenous vitamin C glutathione B-complex HCV
shared by Nathan Goodyear on 25 Sep 13 - No Cached
  • Nathan Goodyear on 25 Sep 13
     
    IV antioxidant mixture of vitamin C, glutathione, glycyrrhiza, and B-complex reduces liver enzymes.  Arm taking only oral shows no decline in liver enzymes.
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High Dose Vitamin C Therapy for Fever of Unknown Origin: A Case Report by Journal of Or... - 0 views

issuu.com/...1 infection vitamin C fever
shared by Nathan Goodyear on 13 Aug 19 - No Cached
  • Nathan Goodyear on 13 Aug 19
     
    Oral vitamin C used to treat a child with a fever of unknown origin none responsive to antibiotics.
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Intravenous Ascorbate as a Tumor Cytotoxic Chemotherapeutic Agent - 0 views

www.seanet.com/...d_hypotheses_1995-v44-p207.htm vitamin C cancer IV vitamin C ascorbic acid
shared by Nathan Goodyear on 05 Mar 18 - No Cached
  • There is a 10 — 100-fold greater content of catalase in normal cells than in tumor cells
  • induce hydrogen peroxide generation
  • Ascorbic acid and its salts (AA) are preferentially toxic to tumor cells in vitro (6 — 13) and in vivo
  • ...36 more annotations...
  • related to intracellular hydrogen peroxide generation
  • only be obtained by intravenous administration of AA
  • Preferentially kills neoplastic cells
  • Is virtually non-toxic at any dosage
  • Does not suppress the immune system, unlike most chemotherapy agents
  • 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
  • Strengthens the structural integrity of the extracellular matrix which is responsible for stromal resistance to malignant invasiveness
  • 1969, researchers at the NCI reported AA was highly toxic to Ehrlich ascites cells in vitro
  • In 1977, Bram et al reported preferential AA toxicity for several malignant melanoma cell lines, including four human-derived lines
  • Noto et al reported that AA plus vitamin K3 had growth inhibiting action against three human tumor cell lines at non-toxic levels
  • Metabolites of AA have also shown antitumor activity in vitro
  • 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
  • the normal cells grew at an enhanced rate at the low dosages (1.76 and 3.52 mg/dl)
  • 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.
  • No toxicity or inhibition was demonstrated in the normal, human skin fibroblasts (ATCC CCD 25SK) even at the highest concentration of 50 mg/dl.
  • the use of very high-dose intravenous AA for the treatment of cancer was proposed as early as 1971
  • 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
  • AA, plasma levels during infusion were not monitored,
  • 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
  • This low cytotoxic level of AA is exceedingly rare
  • 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
  • normal range (95% range) of 0.39-1.13 mg/dl
  • 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
  • plasma levels of over 100 mg/dl have been maintained in 3 patients for more than 5 h using continuous intravenous infusion
  • 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
  • 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.
  • 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
  • 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.
  • Klenner, who reported no ill effects of dosages as high as 150 g intravenously over a 24-h period
  • Cathcart (55) who describes no ill effects with doses of up to 200 g/d in patients with various pathological conditions
  • following circumstances: renal insufficiency, chronic hemodialysis patients, unusual forms of iron overload, and oxalate stone formers
  • 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
  • any cancer therapy should be started at a low dosage to ensure that tumor hemorrhage does not occur.
  • patient is orally supplementing between infusions
  • 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
  • Every effort should be made to monitor plasma AA levels when a patient discontinues intravenous AA therapy.
  • Nathan Goodyear on 05 Mar 18
     
    Older study, 1995, but shows the long-standing evidence that IVC preferentially is cytotoxic to cancer cells.`
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Oral vitamin C reduces arterial stiffness and platelet aggregation in humans - PubMed - 0 views

pubmed.ncbi.nlm.nih.gov/10547085 platelets vitamin C
shared by Nathan Goodyear on 22 Nov 21 - No Cached
  • Nathan Goodyear on 22 Nov 21
     
    Vitamin C reduces platelet agglutination.
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Pharmacokinetics of Vitamin C: insights into the oral and intravenous administration of... - 0 views

diigo.com/0fdt8y IV vitamin C cancer vitamin C pharmacokinetics
shared by Nathan Goodyear on 21 Aug 19 - No Cached
  • Nathan Goodyear on 21 Aug 19
     
    to be read.
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Ascorbate in pharmacologic concentrations selectively generates ascorbate radical and h... - 0 views

www.ncbi.nlm.nih.gov/...PMC1885574 vitamin C ascorbic acid Cancer
shared by Nathan Goodyear on 05 Mar 18 - No Cached
  • Proposed mechanism
  • The data show that pharmacologic ascorbate concentrations produced Asc•− selectively in extracellular fluid compared with blood and that H2O2 formation occurred when Asc•− concentrations were >100 nM in extracellular fluid.
  • These data validate the hypothesis that ascorbate is a prodrug for selective delivery of reactive species to the extravascular space
  • ...22 more annotations...
  • pharmacologic ascorbate as a prooxidant drug for therapeutic use.
  • Recently we reported that pharmacologic ascorbic acid concentrations produced H2O2 concentrations of ≥25 μM, causing cancer cell death in vitro
  • We found that H2O2 concentrations generated in vivo were those that caused cancer cell death in vitro
  • When ascorbate was given parenterally, Asc•−, the product of a loss of one electron from ascorbate, was detected preferentially in extracellular fluid compared with blood
  • Asc•− generation in extracellular fluid depended on the ascorbate dose and the resulting concentrations
  • With i.v. administration of ascorbate, Asc•− concentrations were as much as 12-fold greater in extracellular fluid compared to blood and approached 250 nM
  • In blood, such Asc•− concentrations were never produced and were always <50 nM
  • These data are all consistent with the hypothesis that pharmacologic ascorbate concentrations in vivo serve as a prodrug for selective delivery of H2O2 to the extracellular space
  • After oral ingestion, control of intracellular and extracellular ascorbate concentrations is mediated by three mechanisms: intestinal absorption, tissue transport, and renal reabsorption
  • intestinal absorption, or bioavailability, declines at doses >200 mg
    • Nathan Goodyear
      Nathan Goodyear on 05 Mar 18
       
      significant limitation of gut absorption of vitamin C--at 200 mg po.
  • corresponding to plasma concentrations of ≈60 μM
    • Nathan Goodyear
      Nathan Goodyear on 05 Mar 18
       
      equates to 0.06 mM.  Max blood levels found with po AA dosing has been 0.22 mM
  • at approximately this concentration, the ascorbate tissue transporter SVCT2 approaches Vmax, and tissues appear to be saturated
    • Nathan Goodyear
      Nathan Goodyear on 05 Mar 18
       
      SVCT2 Rc in gut reach max binding.
  • also at ≈60 μM, renal reabsorption approaches saturation, and excess ascorbate is excreted in urine
  • Parenteral administration bypasses tight control
  • When tight control is bypassed, H2O2 forms in the extracellular space
  • in vivo validation of ascorbate as a prodrug for selective H2O2 formation
  • Temporarily bypassing tight control with parenteral administration of ascorbate allows H2O2 to form in discrete time periods only, decreasing likelihood of harm, and provides a pharmacologic basis for therapeutic use of i.v. ascorbate
  • H2O2 formation results in selective cytotoxicity
  • Tumor cells are killed with exposure to H2O2 for ≤30 min
  • In vitro, killing is mediated by H2O2 rather than Asc•−
  • In addition to cancer treatment, another potential therapeutic use is for treatment of infections. H2O2 concentrations of 25–50 μM are bacteriostatic
  • virally infected cells may also be candidates
  • Nathan Goodyear on 05 Mar 18
     
    follow up invivo study to previous study from 2005.  Here, the authors prove their hypothesis that ascorbate is a prodrug for delivery of H2O2.
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