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  • Aim: There is growing interest in pharmacologic ascorbate (Asc) and its therapeutic properties (Levine et al. Adv Nutr 2011;2:78). W e examined cell viability, histone deacetylase (HDAC) expression, and related protein modifications in cancer versus non- cancer colon epithelial cells following exposure to Asc. Methods: MTT assays were conducted in HCT116 colon cancer and CCD841 non-transformed colonic epithelial cells treated with 0.25 to 16 mM Asc or ascorbate-2-phosphate (AAp), in the presence and absence of catalase (CAT, 280 U/mg), or with 5 to 160 μM H₂O₂. Cell lysates obtained 6 h and 24 h post-treatment were immunoblotted as reported by Rajendran et al. Mol Cancer 2011;10:68. Results: In MTT assays, IC₅₀ data were as follows: 8 mM Asc (CCD841); 3 mM Asc (HCT116), >50mM AAp (HCT116), and 65 μM H₂O₂ (HCT116). CAT protected against both Asc- and H₂O₂- induced cytotoxicity. At 6 h, Asc and H₂O₂ altered the expression of HDACs (HDAC4, HDAC6, SIRT3) and enhanced the acetylation of histone (H3, H4) and non-histone proteins (tubulin, p53). Conclusions: Asc was more cytotoxic to colon cancer cells than non-cancer cells. Findings with the non-H₂O₂ producing compound AAp, and with CAT, implicated H₂O₂ in Asc-induced cytotoxicity. Asc was shown, for the first time, to alter epigenetic end-points related to HDAC changes in colon cancer cells.
  • Keywords: Epigenetics, Vitamin C, Kaiser, Linus Pauling Institute, Ascorbate, Cancer, HDAC
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