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
We have noted previously the capacity of chloride ions to bind fatty acids. The bond represents the first step in abnormal metabolism of sodium chloride. In a second step, sodium forms alkaline compounds by binding with the carbonate anion and, in sufficient amounts, induces local alkalosis. Accumulated in cells along with water, the sodium compound leads to the appearance of vacuoles. In interstitial fluid, the same process induces edema and pain of an alkaline pattern. At the systemic level, it results in a state of shock.
In the last analysis, the influence of the alkaline sodium compounds can be considered to result from the lack of anions other than carbonate available to bind sodium. For this reason, we were interested in studying the effects of substances able to furnish the chloride anion to the organism. Through metabolism of ammonium chloride and calcium chloride, chloride ions are liberated in the body. They have little effects at lower levels. An immediate influence on local pH is seen at the tissue level. Favorable influence on alkaline pain is part of this action. The effect of ammonium chloride in shock is related to the fact that it furnishes the needed chloride ions.
The action of chloride upon alkaline sodium compounds, however, is handicapped by another aspect of its intervention. Studies of the pathogenesis of shock has shown a noxious effect produced by compounds resulting from the bond of chloride ions to fatty acids. The gastric ulcerations seen in the state of shock with the severe liver damage produced by several chlorine compounds—could be largely related to the bond of chloride ions to fatty acids. This led to the idea of trying such combinations in vivo to destroy abnormal entities such as tumoral cells. By using lipoids rich in chlorides, we hoped to achieve this without the noxious effect of free sodium ions.
We administered trichlorethylene and chlorbutanol (the last also used as an antiseptic in many pharmaceutical preparations). No effect was seen at any level in experiments on animals and humans. In a second step, we added chlorine to various lipoids, especially those with negative polar groups. We started with 9, 10-dichlorostearic and 9, 10, 12, 13-tetra chlorostearic acid. The results with these preparations in animals and in a few humans were not encouraging. Investigation of products obtained through fixation of chlorides at the double bond of conjugated fatty acids, has shown that, in large amounts, they are able to induce gastric ulcerations in rats and rabbits. This brought us back to the use of chlorides as anti D agents—of which sodium chloride appears to be the most effective.
In another series of experiments, we tried to replace the chloride ion with another halogen. We studied the influence of fluorine, bromine and iodine compounds, this time upon the processes that induce abnormal patterns related to predominance of abnormal fatty acids. The administration of sodium fluoride and of other compounds containing fluorine did not have any appreciable effect either in animals with tumors or other pathological conditions, or in humans with alkaline pattern of pain. The fact that fluorine belongs to the organism level led us to investigate it in terminal cases. Neither pain nor tumor evolution was changed. Bromine, too except for a sedative effect, did not influence systemic changes, pain or tumor growth.