# Magnetic Fields Trump Oxygen in Controlling the Death of Erythro-Leukemia Cells
## 4 Discussion
Since checkpoints in the apoptotic process include verification of ATP supply [25], demands on ATP by physiological adaptations retarded the apoptotic process, reducing the late/early apoptosis ratio. This delay in apoptosis, coupled with ROS stress, diverted some of the cells undergoing apoptosis under MF Transitions to necrosis [26]. Our previous work [7] as well as that of others [27; 28] has shown that EMR perturbs the movement of free electrons and protons along the OXPHOS chain of enzymes (Complex I to V). Complex V, otherwise known as ATP synthase, is itself a serial system, dependant on the tunneling of protons through a channel containing a string of 10 molecules of water [29]. EMR reduces the transparency of ATP synthase channels, increasing the mitochondrial membrane potential (\(\Delta\Phi\)m). This increased \(\Delta\Phi\)m pushes cells towards a cancer phenotype [30; 31; 32], resulting in documented changes in growth rate, morphology, survival rate and chromosome numbers in cancer cells [7]. Many of our observations support the inhibition of OXPHOS and ATP synthesis by MFs. 1. \"Zero\" MF conditions (facilitated ATP synthesis) should favor a higher late/early apoptosis ratio. Table 2 shows that this is true for baseline cultures at both High (2.43 \(>\) 1.23) and even Low (1.66 \(>\) 1.51) oxygen. 2. The hypoxic Zero MF Transition of Table 4 had the highest late/early apoptosis ratio (10) of any Transition. When Incubator fields were applied to the same hypoxic Transition, the late/early apoptosis ratio fell by 23%. 3. Although hypoxia was effective at inducing apoptosis (5.2, 5.3, 3.3, 2.71 in Table 4), to induce it quickly, as shown by a high late/early ratio, the MF must be unchanging (10, 7.74). This rapid apoptosis was almost completely inhibited (1.26, 1.04 in Table 4) if a MF change was superposed, constraining ATP resources. 4. Transitions columns in Table 4 are ordered from left to right by decreasing necrosis rating. In the left half of the Table (high necrosis), all MFs are changing, except in two cases, which correspond to hyperoxic rises. Larger shifts in cellular environments, as simultaneous oxygen and MF changes, placed a heavier adaptive load on cells, requiring 5\({}^{\prime}\)-adenosine monophosphate-activated protein kinase alpha (AMPK to manage more adjustments [33]. These requirements slowed apoptosis, and increased necrosis (left side of Table 4). 5. Table 3 shows that that the rush to late apoptosis of the hypoxic Transitions with no MF change (2.4, 3 in Table 3) attenuated necrosis (0.48, 0.49 in Table 4) by simple apoptosis to necrosis competition. This indicates that MF variations switch cell death from apoptosis to (inflammatory) necrosis. But under hyperoxic \"Zero\" MF, the hyperoxia actually attenuated apoptosis (necrosis/apoptosis = 2.6), which means that hyperoxia, through ROS, was quickly toxic to the apoptotic pathway [34], shifting cells towards necrosis. Mitochondrial perturbations, and changes in the mechanisms of cell death (necrosis vs. apoptosis) are considered relevant or causative for chronic human diseases such as diabetes [33; 35; 36], heart disease [37; 38; 39], and diseases of post-mitotic tissues such as Parkinson's [40; 41], Alzheimer's [42; 43; 44], multiple sclerosis, amyotrophic lateral sclerosis [45], autism [46], and psychiatric disease [47]. Tissues with high metabolic rates such as the brain [48; 49], physiological systems with an already high ROS load [50] such as the islets of Langerhans [51; 52], and processes of sperm formation [53] would be particularly vulnerable. It is not unexpected that environmental EMR exposures would impact many human diseases [54], because undermining ATP supply and the stability of its regulation connects directly to ROS. When the foundations of a building are de-stabilized, many rooms can feel the tremor. A better perspective on MF effects in our environment will emerge as more diverse cell models are investigated.