This section is from the book "Research In Physiopathology As Basis Of Guided Chemotherapy With Special Application To Cancer", by Emanuel Revici. Also available from amazon: Research In Physiopathology
Copper, from the IB series and another anti A element of the cellular level, appears indispensable for the synthesis of heme of catalase. A deficiency of copper results in reduced activity of this enzyme. Similarly, the synthesis of hemoglobin is possible only in the presence of copper. Cytochrome oxidase contains Fe and Cu. Cu deficiency reduces liver cytochrome oxidase. (150, 151, 152) Cu is present in blood serum bound to a protein to form ceruloplasmin which also acts as an oxidase. (153) Cu, while favoring the synthesis of these substances, intervenes ultimately in the processes which lead to the active catabolic intervention of oxygen. In this way, Cu acts as a D inducing agent. Cu intervenes actively in the metabolism of sulfur. (154, 155) The transformation of sulfhydryl to disulphide is slow and incomplete when there is a copper deficiency. The same deficiency reduces the formation of phospholipids as seen in rat liver. (156) Indirectly, Cu favors anti A activities.
The influence of Cu upon Ca metabolism also is indirect. We have seen that a local deposit of calcium in bones corresponds to a local D pattern. Deficiency in copper, a D inducing agent, permits the appearance of local A conditions, which in the case of bone, will result in a lack of calcium, the opposite of what is seen in local D offbalance. This correlation explains why, in spite of sufficient P and Ca, the lack of copper induces an osteomalacia with bone fracture and symptoms of rickets, as seen in animals with an indirect Cu deficiency caused by an excess of molybdenum, (157, 158, 159) an A inducing agent. The administration of copper helps to repair these fractures. (157) Parallel reductions in Cu and Mg occur in milk fed calves. (160) A richness of zinc, like molybdenum, can provoke a deficiency in Cu and Ca. With copper deficiency and low catalase, resistance to infections is lowered. In brucellosis, a deficiency of Cu and Ca coincides with reduced concentrations of Mn and Co in the blood and pituitary glands. (161, 162, 163) Cu, Ca, Mn and Co are all metals of the D inducing group.
In cancer, a qualitative deficiency of copper is found. A frank reduction of the catalase content is seen in cancerous cells as well as in the liver of cancerous subjects. (164, 165) On the other hand, Cu content is considerably increased in the blood of these subjects, with values even three times greater than normal, often encountered. (166, 167, 168) These values return to normal if the cancerous tumor disappears. (169)
In cancer, copper deficiency at the level of the cells is manifest, shown not only by reduced catalase but also by upsets in the cytochrome oxidase system, the heme system, the SH metabolites, and the phospholipids. The deficiency, however, is only local and consequently qualitative since an excess of Cu is found at the immediately superior level, the blood.
A local abnormality residing in inadequate capacity to utilize copper thus appears related to cancer. In normal animals, copper in excess can be utilized and is able to prevent the appearance of tumors. This explains why Cu, which protects rats against carcinogenetic azodyes, (170, 171, 172) does not influence the tumors once they have been induced, i.e., once the qualitative insufficiency is present. The recognition of this difference between the form in which copper is utilized by the normal animal and the deficiency in the cancerous entities, has been the basis for a series of studies concerning this key problem in the pathogenesis of cancer. The therapeutic use of copper—and of other elements which we will discuss below—is not a quantitative but a qualitative problem.