5. Conclusions

We studied the ChemIndHep experimentally through the use of MRHM. We found that the periodical application with ELF-EMF (4.5 mT (120 HZ)) inhibits by more than 50% the number and area of GST-P liver foci and preneoplastic liver lesions in rats. Through the reduction of cell proliferation and without alteration of the apoptosis process, ELF-EMF interferes with the altered cell cycle continuity and DNA synthesis induced by ChemIndHep. Theoretically, we found that with the use of a 120 Hz ELF-EMF it was possible to achieve modulation of the magnetic-sensitive short-lived RP intermediaries produced by the OS, generated when xenobiotics are metabolized during the catalytic cycle by the CYP450 in the early ChemIndHep. The process of modulation uses the competitive kinetics of the RP selective reactions [71], giving the role of a molecular motor to the enzymatic protein [9]. To achieve this, we studied a quantum mechanics model to describe the interaction of RP/hepatocytes following the typical Haberkorn approach studying the spin dynamics and employing the path integral method and second quantization. The idea of this chapter was to obtain an explanation of the way in which hepatocytes can modify their electronic structure when interacting with the RP, which comes from the enzymatic reaction. Although it is an in-depth mathematical model, the results of our research provide us with further details of the MF's control on BS, specifically in the ChemReac that modulates the electrons in OS (cytoprotective effect) generated in the reactive hepatocytes-RP system in the liver, with the outcome of understanding hepatocarcinogenesis.
