AbstractsMedical & Health Science

A biological assay based on human cancer cells was developed as an index of metabolic state. This assay is used here to describe the metabolic actions of a variety of agents: oxygen, melatonin, vitamin C, the drugs oligomycin and imatinib, as well as extra-low frequency (ELF) magnetic fields (MFs). Based on chromosome counts in cancer cells, it led us to uncover a basic mechanism of interaction between ELF MFs and biological materials. The action of MFs is through an alteration of the structure of water originally described by Russian physicists at Lomonosov University in Moscow, in the early 1980s. As is the case in many projects, our work started as a fundamental investigation, specifically of the effects of oxygen on cancer cells in culture.Chromosome counts above 46 are observed in the majority of human tumours. But while real tumours grow in oxygen and nutrient restricted environments, cultured cancer cells are provided with 21% oxygen and generous nutrition, stimulating their metabolism. We studied the connection between metabolic activity of cancer cells and their chromosome counts, observing that five metabolic restrictors induced catabolism and chromosome losses in five hyperploid cancer cell lines. These karyotype contractions allow cancer cells to support fewer chromosomes, increase their proliferation rate and acquire the phenotype of a stable, growing tissue. Hyperploid cancer cells expand or contract their karyotypes through rapid mechanisms of endo-reduplication or chromosome loss. These fast meta-genetic mechanisms explain the surprising adaptability of tumours to changing micro-environments and therapeutic interventions. Furthermore, karyotype contraction may provide a basis for the previously observed carcinogenic action of some anti-oxidants, positioning metabolic restriction as a meta-genetic mechanism of tumour promotion.Biological effects of ELF MFs have lacked a credible mechanism of interaction between fields and living material. The effect of ELF MFs was evaluated in our human cancer cell cultures. Ultimately, five cancer cell lines were exposed to ELF MFs within the range of 0.025 to 5 µT, and were examined for karyotype changes after 6 days. Similar to the chemical metabolic restrictors, all cancer cells lines lose chromosomes from MF exposure. MFs from 25 nT to 5 µT reduce the chromosome counts, with a mostly flat dose-response. Constant MF exposures for three weeks allow a rising return to the baseline, unperturbed karyotypes. From this point, small MF increases or decreases are again capable of inducing KCs. Our data suggests that the KCs are caused by MF interference with mitochondria's ATP synthase (ATPS), compensated by the action of AMP-activated protein kinase (AMPK). The effects of MFs are similar to those of the ATPS inhibitor oligomycin. They are amplified by metformin, an AMPK stimulator, and attenuated by resistin, an AMPK inhibitor. Over environmental MFs, KCs of various cancer cell lines show exceptionally wide and flat dose-responses, except for those of erythro-leukemia…