By Mark Simon, Director
Nutritional Oncology Research Institute
Mitochondria Targeted Cancer Therapy
To effectively treat cancer and accomplish it with little or no damage to normal healthy cells, specific targets unique to cancer cells must be identified. Off-target damage limits the utility of conventional chemotherapy and radiation. So called targeted therapies target specific cell signaling pathways but affect normal cells as well as cancer cells. The preferred and ideal cancer therapy should target only cancer cells while causing no harm to normal cells or raising the risk for second cancers.
Our cells are a hybrid composed of a main cell and hundreds of mitochondria which are essentially bacterium. Mitochondria contain their own DNA encoding 37 genes largely responsible for energy metabolism. There is crosstalk between nuclear and mitochondrial DNA. Mitochondria regulate apoptosis (natural programmed cell death) and for this reason alone are a primary target in cancer therapy.
Mitochondria are metabolic engines generating the majority of ATP (energy) within a normal cell. Cancer cells exhibit abnormal energy metabolism due to dysfunctional mitochondria. There are two distinct energy generating systems in the mitochondria, the Tricarboxylic Acid (TCA) cycle and the Electron Transport Chain (ETC). The ETC system produces the majority of the energy within a normal cell through a series of reactions called oxidative phosphorylation (OxPhos). Oxygen is consumed in these reactions.
The mitochondria in cancer cells are damaged and dysfunctional locking the cell in an endless replication process. Causing further damage to already damaged mitochondria releases the signals for apoptosis. Many natural compounds are available to induce the necessary level of mitochondrial damage to only cancer cells while sparing normal healthy cells. Overwhelming the cancer cell with oxidative stress accomplishes the task of triggering apoptosis. Cancer cells are already under a very high oxidative stress level due to their altered metabolism and mitochondrial dysfunction. A little extra oxidative stress pushes the cancer cell over the cliff and it self destructs. Hydrogen peroxide is an example of an agent capable of inducing excess oxidative stress. Sodium selenite is another. Most natural ant-cancer agents generate reactive oxygen species (ROS) within cancer cells which will surely trigger apoptosis.
NORI utilizes combinations of natural agents directly targeting mitochondria and triggering apoptosis. A novel combination of taurine, zinc, sodium selenite and vitamin K3 is undergoing evaluation. There are potentially hundreds of synergistic combinations of nontoxic agents that can be very effective in selectively killing cancer cells. NORI chooses agents from a long list based on good bioavailability, long half life, low therapeutic concentration threshold and low-cost. What is common among the various combinations (cocktails) is the generation of oxidative stress (ROS) that causes the collapse of mitochondrial function which triggers apoptosis. Normal cells are unaffected because of a much lower oxidative stress baseline.
Diet has little or no direct effect on mitochondria. Avoidance of antioxidant supplements is helpful in lowering cancer cell’s ability to manage oxidative stress. A 100% plant-based low-fat diet is always recommended for cancer prevention and during treatment. Never rely on diet alone to manage cancer. Much more is required including high dose nutraceuticals, hormonal therapy and conventional treatments where appropriate.
Weinberg, Samuel E, and Navdeep S Chandel. “Targeting Mitochondria Metabolism for Cancer Therapy.” Nature chemical biology 11.1 (2015): 9–15. PMC. Web. 23 Feb. 2018.
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