Injections of Substances Inducing Apoptosis to Cancer Cells but Stimulation of Normal Cells May Prevent Cancer

Selenium（Se） compounds have prevented and Se-deficiency has induced the initiation of cancer. Se（0）-forming compounds and hydroxy-xanthones have killed cancer ceils but shown beneficial effects to normal cells. They may together be effective in the treatment of cancer. Many enzymes which contain selenocysteine （Secys） can catalyze reactions with reducible oxygen （O2~ 02 or H202）. Experiments strongly support that Se-enzymes are activated by Se（0）, from e.g. selenite, selenodiglutathione, binding to Se（-II） in Secys, forming an electron conducting Se-link to reducible oxygen as a protection against oxidations. Cancer cells, which are energy supported only from fermentation, are not dependent on Se which is why they are more sensitive to toxic effects of Se than normal cells. The energy from fermentation is insufficient for normal cell functions. High doses of Se（0）-containing compounds are toxic in that they form links with thiols （R-S-Se） reducing their reaction rate. The reaction of an SH-enzyme, necessary in fermentation, is impaired. Mangostins （hydroxy-xanthones） induce apoptosis in human cancer ceils but stimulate respiration. The OH-groups are responsible for the effects and the reduction of NADP＋ into NADPH. Fermentation is inhibited as NADP＋ is necessary for the process. Cancer may be treated by injections of Se（0）-forming compounds and hydroxy-xanthones into cancer cells in doses causing apoptosis. However, in diluted form, when meting normal cells, the substances promote the yield of energy by stimulating the electron transference to reducible oxygen. Se（0）-activated Se-links and hydrogen from hydroxy-xanthones hopefully prevent the initiation of cancer.

The Conditions for Se-Enzymes, NO, cGMP and LDL to be Formed and How They are Connected with Each Other

Transportation of energy and substances is fundamental for the conditions of life. The energy from metabolised food is yielded at the reduction of oxygen by the assistance of Se-enzymes. Activated Se-enzymes contain an electron conducting Se-link with elemental Se bounded to Se-cys （Se-cystein） that prevents electron transferring （autoxidable） agents, as arginine, from oxidations. NO is formed from e.g. arginine during the passive state of a Se-enzyme. With NO, instead of O2, bounded to a hem group, destroying oxidations are avoided. This is the role of NO. A nerve signal is activated by the GTP （guanosine triphosphate）-induced triggered transformation of cGMP （cyclic guanosine monophosphate） into GMP, closing the sodium channels. When GTP is consumed, the opposite reaction takes place. The direct influence of the GMP/cGMP quote on a nerve signal makes GMP/cGMP equal to EDHF （endothelium-derived hyperpolarizing factor）. Part of the energy from food is stored and transported in the form of acetyl groups, building up many important molecules of which LDL （low density lipoprotein） is one, containing cholesteryl esters. These are brought in to the cell, decomposed to acetyl groups generating hydrogen, H, making LDL to an essential substance. High levels are connected to impaired energy yielding reactions, perhaps related to low levels of some substances, especially to one or both forms of Se. The necessity of a Se-link and NO induced protection against oxidations by reducible oxygen can no longer be neglected.