Abstract
Tumor extracellular acidity is a hallmark of malignant cancers. Thus, in this study we evaluated the effects of the oral administration of a commercially available water alkalizer (Basenpulver®) (BP) on tumor growth in a syngenic melanoma mouse model. The alkalizer was administered daily by oral gavage starting one week after tumor implantation in CB57/BL mice. Tumors were calipered and their acidity measured by in vivo MRI guided 31P MRS. Furthermore, urine pH was monitored for potential metabolic alkalosis. BP administration significantly reduced melanoma growth in mice; the optimal dose in terms of tolerability and efficacy was 8 g/l (p< 0.05). The in vivo results were supported by in vitro experiments, wherein BP-treated human and murine melanoma cell cultures exhibited a dose-dependent inhibition of tumor cell growth. This investigation provides the first proof of concept that systemic buffering can improve tumor control by itself and that this approach may represent a new strategy in prevention and/or treatment of cancers.
Highlights
The tumor acidic microenvironment is a highly hostile milieu that poses a challenging riddle to clinical researchers
The high acidity was instrumental to induce the solubility of the alkaline supplement since the carbonate that is present within the alkalizing mix has a poor water solubility at pH values approaching neutrality
We wished to evaluate if BP at the concentration of 8 and 16 g/l could affect the viability of different melanoma cell lines (Mel 501, B16F10, A375, Me30966 and WM793)
Summary
The tumor acidic microenvironment is a highly hostile milieu that poses a challenging riddle to clinical researchers. This acidity is the result of the abnormal glucose consumption by tumor cells [1,2,3]. ATP production by glycolysis is more rapid than by oxidative phosphorylation, it provides a much lower energy gain. This handicap leads to the cancer cells greatly increasing their glucose uptake to meet their amplified energy, biosynthesis and redox requirements, resulting in lactate accumulation and the disposal of this end product
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