Neoplastic Amplification---New Insights

Outstripping the oxygen supply within a tumor probably favors an increase in thiols through less monooxygenase-dependent oxidation of thiols to disulfides and other regulatory oxidative intermediates. The resulting thiol-dependent proliferation of both tumor and normal cells places even more pressure and nutrient demands upon an already restricted blood supply in the vicinity of the tumor.

Lysing of cells in the necrotic centers of tumors causes the loss of intracellular anti-oxidants, such as glutathione. The remaining membranous ghosts of the cells, when released into the blood stream and reoxygenated, are more susceptible than intact cells to lipid peroxidation. Lipid epoxides react with thiols, and could easily eliminate the minute amount of thiol, such as vitaletheine, needed to generate an oxidative regulatory response. Such a scenario might explain the importance of the immune system's ability to eliminate cell debris through phagocytic processes and the results obtained when dead tumor cells were co-administered with vitaletheine modulators.

Lipid peroxidation might also increase the background noise for oxidative signals controlling cell proliferation by falsely signaling that too much of the specific oxidative signal is being generated. A compensatory scaling back of the specific oxidative signal would theoretically cause an additional undesirable increase in thiol-dependent proliferation of cells, further compounding the neoplastic problem. Based upon this rationale, lipid-soluble antioxidants are natural choices for helping to control cancer by preventing this high background noise in oxidative signaling.

As predicted by the ability of many metal toxins to bind sulfur in the thiol (mercaptan or free sulfide) form, and in so doing inactivate vitaletheine, it is becoming more and more evident that people with intractable cancers are poisoned by toxic metals. Thus, DEtoxing is extremely important in the long-term prognosis for survival of these individuals.