In one case, organic acids are formed during respiration and are products of incomplete oxidation of sugar. Such acids from Sugars are gradually reduced to their final products: carbon dioxide and water. The release of free acids beyond the Krebs cycle is not here.
In another case, organic acids-the starting building material for the synthesis of a variety of compounds — carbohydrates, amino acids and fats. In this case, free acids can be formed, leaving the cytoplasm and playing various roles there. On the one hand, they are metabolites of both respiration and catabolism, and on the other — a substrate for anabolism. The highest form of respiratory processes are carried out in the mitochondria, and simple glycolysis can take place in the cytoplasm.
There are acids that can be predominantly a product of the anaerobic fermentation process, such as lactic acid. There is a group of acids that are a product of aerobic metabolism. It can be assumed that some acids, which are the product of the anaerobic process, are not suitable for our purposes, as they will only aggravate the situation, because their cancer cells already produce in excess. Obviously, this is a free acid outside of the cell. At the same time, there are practically no substances that are not interchangeable in the process of metabolism: any type of acid can be a mediator of anabolism and catabolism.
For practical purposes, the question is important: how to accelerate the processes of catabolism in cancer cells with the help of acids? In seeking an answer, it is appropriate to consider separately all the evidence against this, as well as the arguments in favor of our assumption.
The arguments against the fact that using acids can be enhanced catabolic processes in the cancer cells.
Normally, in systems striving for stability, they are usually always balanced. Shifts are possible only, for example, under the influence of hormones. It could be assumed that the acceleration of catabolism in the tumor should logically lead to an automatic increase in anabolism, and Vice versa. This raises doubts about the possibility of provoking catabolism in tumors.
Doubt about the possibility of a focal metabolic roll in the tumor area with the help of acids can also cause the assumption about the universalism of metabolism, i.e. the principle possibility of interchangeability of substrates: organic acids, carbohydrates, proteins, lipids.
As substances for energy and synthesis of new substances (assimilation and anabolism), cells can in principle use both organic acids and alkaline substances. In this regard, cancer cells do not differ from the usual. Everything is interchangeable and regulated by the needs of the tissue as well as the body as a whole. Therefore, acids in different situations can be used for energy, i.e. breathing, as well as for synthesis and growth processes. One would assume that a surplus of acids in the tumor can lead to the restructuring of the metabolism of tumor cells and the transition to a state of growth, anabolicbodies. In addition, even in conditions of starvation, when the body automatically switches to catabolism, the tumor is able to selectively intercept even small residues of metabolites, constantly secreted by other tissues. This means that it is not necessarily unambiguously that the tumor will be oversaturated with acids.
It could be assumed that the substrate it feeds on is less important for the tumor, and the need for continuous unregulated growth is more important. Obviously, there is an analogy with some types of unicellular bacteria that can actively grow in one case on acidic media, and in the other — on alkaline: glycerin, alcohol, sugar, etc.
The genome of cells of higher animal organisms has a full set of genes for the existence of both different acidic environments and different alkaline. In principle, tumor cells could exist on media of the opposite type.
All said requires to consider the characteristics of oncolytic metabolism and its interaction with the metabolism of the body.
One example of substrate interchangeability is neoglucogenesis . The connection of mechanisms of neoglucogenesis could mean that forcing the processes of catabolism in the tumor would always have limitations due to the formed “hole”, leakage, when energy processes flow from one type of substrate to another.
But the transition of cancer cells on a new type of substrate leads to a forced transition to a new implementation programme of the energy sector. Obviously, this is an important point, as in the mitochondria begin to connect new gene lines, not spoiled yet for any reason. Connection to the mitochondria starts the whole complex of programs in the genome of the nucleus of cells. Runs a huge number of adjustment programs that work normally and inhibit the unregulated growth of cancer cells.
It can be assumed that such a situation could exist in encoding only during inflow of acidic substrate. Undoing this imbalance would lead onkokletki in the opposite state. But nevertheless, the fact of resorption of tumors is known, and it is obvious that it should be associated with the gradual repair of diseased cells, the restoration of clonal offspring with normal mitochondria and membranes. IPT may include mechanisms of elimination, culling of such cells.
I want to note at once that such interchangeability of substrates is really easily carried out in healthy tissues, striving to preserve their stability, balance of metabolism. At the same time, for cancer cells to maintain such resistance on different substrates is much more difficult, given their aggressive “voracity” and wastefulness, waste substrates, the output of a huge amount of waste products half-life: they have to spend more, in order to at least something to re-create. With a lack of certain substances they begin to dominate the processes of catabolism over anabolism.
Doubt can also cause the possibility that the tumor can be locally put on the path of catabolism. This is due to the assumption that in the conditions of lack of supply of substrates, the tumor can still dominate and intercept everything until the last. Also, it can destroy the surrounding tissues with its metabolites and cause catabolism in them, and then intercept the products of their catabolism and translate into their metabolism through the mechanisms of neoglucogenesis. Let me remind you of the following fact: even in conditions of medical starvation, the tumor continues to grow actively, which really confirms our assumption. The challenge here obviously is solved only in roundabout ways.
- It is necessary to force the tumor to allocate minimal catabolite metabolites — this can be achieved by excessive use of antioxidants and oxygenators.
- Oversaturate the body and the tumor with organic acids so that the saturation gradient of the substrate field is higher than the intake of other substrates “coming” from other tissues as a result of catabolism processes in them.