Potential Therapeutic Application of the Association of Vitamins C and K3 in Cancer Treatment

P.   Buc   Calderon; J.      Cadrobbi; C.      Marques; N.      Hong-Ngoc; J.   M.   Jamison; J.      Gilloteaux; J.   L.   Summers; H.   S.   Taper

Abstract

The decision of stressed cells to die or to survive is made by integrating signals at different levels through multiple check points. However, initiation and continued progression toward cell death by apoptosis in cancer cells may be blocked by mutation of the tumor suppressor p53 or overexpression of members of the bcl-2 family of proteins. The existence of such mechanisms indicates that cancer cells lose the controls regulating their cell cycle. Therefore, the activation of their programmed cell death appears as a major therapeutic target. Oxidative stress can stimulate growth, trigger apoptosis, or cause necrosis depending upon the dose and the exposure time of the oxidizing agent. A large body of evidence supports the idea that oxidative stress induced by redox cycling of vitamins C and K3 in association surpasses cancer cellular defense systems and results in cell death. The molecular mechanisms underlying such a process are, however, still unknown. Indeed, several types of cell death may be produced, namely autoschizis, apoptosis and necrosis. Combined vitamin C and K3 administration in vitro and in vivo produced tumor growth inhibition and increased the life-span of tumor-bearing mice. CK3-treatment selectively potentiated tumor chemotherapy, produced sensitization of tumors resistant to some drugs, potentiated cancer radiotherapy and caused inhibition of the development of cancer metastases without inducing toxicity in the host. We propose the association of vitamins C and K3 as an adjuvant cancer therapy which may be introduced into human cancer therapy without any change in the classical anticancer protocols, and without any supplementary risk for patients.

Keywords: cancer, oxidative stress, apoptosis, autoschizis, ascorbate(vitamin C), menadione(vitamin K3)

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