I am posting this only because Linus Pauling is so vilified and mocked by mainstream medicine. In fact, his proposal to use high doses vitamin C for cancer treatment is listed on QuackWatch as one of the greatest medical hoaxes of the 20th century.
The Dark Side of Linus Pauling's Legacy
Well, it looks like Linus may have the last laugh. This recent study found that very high doses vitamin C, achievable only through injection of IV infusion increase hydrogen peroxide inside the tumor cells and the resulting excessive oxidative stress kills the tumor cells. Pauling repeatedly said that only very high doses of vitamin C are likely to have an effect because lower doses act as an anti-oxidant while higher ones as oxidant, and this is what the study found. Tumor cells surround themlseves with antioxidants like NAC and do everything possible to avoid oxidative stress and ROS like H2O2.
http://www.sciencedirect.com/science/article/pii/S2213231716302634
"...The data presented here quantitatively establish a central role for H2O2, generated upon the oxidation of P-AscH−, in the cytotoxic effects of P-AscH− to cancer cells in vitro. Our data quantitatively support the many observations that indicate that the cytotoxicity of P-AscH− to cancer cells observed in vitro is largely due to its generation of H2O2 in the medium (Supplementary Fig. S1) [1], [2], [3], [4], [5] and [9]. Ascorbate delivered at pharmacological concentrations has shown selective toxicity to several different tumor cell types. While this selective cytotoxicity has been observed to be dependent on the generation of H2O2, the mechanism by which this occurs is still under investigation. Several mechanisms for how the H2O2 generated by P-AscH− elicits its cytotoxicity to tumor cells have been hypothesized and examined, for example: DNA damage [3], [13], [52], [55], [56] and [57]; and the depletion of ATP leading to tumor cell death [1], [3], [10], [58] and [59]. H2O2 plays an integral role in the mechanism. However, many other factors can modulate the toxicity of P-AscH−, e.g. KRAS status [3], the level of catalytic metals[60] and [61], the redox status of the intracellular GSSG,2 H+/2GSH redox couple[45] and [62], and the status of NAD [58]. Yun et al. recently extended the observations that ascorbate selectively kills KRAS and BRAF mutant cells [59]; they suggest that P-AscH− has as a target the redox state of GAPDH. However, the mechanism the authors propose does not consider important published data that clearly demonstrate that P-AscH− induces selective oxidative stress and cytotoxicity in cancer cells vs. normal cells by a mechanism involving the production of H2O2. Some of the biochemical reagents used to probe possible mechanism react directly with H2O2, thereby removing it and protecting the cells; see Supplementary Discussion."
The Dark Side of Linus Pauling's Legacy
Well, it looks like Linus may have the last laugh. This recent study found that very high doses vitamin C, achievable only through injection of IV infusion increase hydrogen peroxide inside the tumor cells and the resulting excessive oxidative stress kills the tumor cells. Pauling repeatedly said that only very high doses of vitamin C are likely to have an effect because lower doses act as an anti-oxidant while higher ones as oxidant, and this is what the study found. Tumor cells surround themlseves with antioxidants like NAC and do everything possible to avoid oxidative stress and ROS like H2O2.
http://www.sciencedirect.com/science/article/pii/S2213231716302634
"...The data presented here quantitatively establish a central role for H2O2, generated upon the oxidation of P-AscH−, in the cytotoxic effects of P-AscH− to cancer cells in vitro. Our data quantitatively support the many observations that indicate that the cytotoxicity of P-AscH− to cancer cells observed in vitro is largely due to its generation of H2O2 in the medium (Supplementary Fig. S1) [1], [2], [3], [4], [5] and [9]. Ascorbate delivered at pharmacological concentrations has shown selective toxicity to several different tumor cell types. While this selective cytotoxicity has been observed to be dependent on the generation of H2O2, the mechanism by which this occurs is still under investigation. Several mechanisms for how the H2O2 generated by P-AscH− elicits its cytotoxicity to tumor cells have been hypothesized and examined, for example: DNA damage [3], [13], [52], [55], [56] and [57]; and the depletion of ATP leading to tumor cell death [1], [3], [10], [58] and [59]. H2O2 plays an integral role in the mechanism. However, many other factors can modulate the toxicity of P-AscH−, e.g. KRAS status [3], the level of catalytic metals[60] and [61], the redox status of the intracellular GSSG,2 H+/2GSH redox couple[45] and [62], and the status of NAD [58]. Yun et al. recently extended the observations that ascorbate selectively kills KRAS and BRAF mutant cells [59]; they suggest that P-AscH− has as a target the redox state of GAPDH. However, the mechanism the authors propose does not consider important published data that clearly demonstrate that P-AscH− induces selective oxidative stress and cytotoxicity in cancer cells vs. normal cells by a mechanism involving the production of H2O2. Some of the biochemical reagents used to probe possible mechanism react directly with H2O2, thereby removing it and protecting the cells; see Supplementary Discussion."