# Magnetic Fields Trump Oxygen in Controlling the Death of Erythro-Leukemia Cells
## 4 Discussion  
Necrosis is the most acute form of cell death, the unregulated disposition of cell components. The loss of cell membrane integrity and release of internal cell elements into the extracellular space trigger the immune system, as invading leukocytes and phagocytes produce an inflammatory response. Damaging substances aimed at microbial control are released by leukocytes, which creates collateral damage to surrounding tissues. In contrast, apoptosis is programmed cell death that recycles cellular components. Apoptosis occurs naturally in humans, for example in shaping developing organisms. Excessive apoptosis shrinks organs, whereas an insufficient amount may, in some cases, result in cancer. It is triggered by the extrinsic pathway (FAS), or by the intrinsic pathway, notably by increase in cell stress due to the level of reactive oxygen species (ROS) in mitochondria. It avoids the immune response of necrosis by a sequence of steps: caspase activation, blebbing, cell shrinkage, enzymatic hydrolysis, chromatin condensation, chromosomal DNA fragmentation, mRNA decay, and apoptotic body formation. Inflammation is avoided by absorption of the apobodies by surrounding cells. Apoptosis typically cannot stop once it has begun, but can be found in various stages in cells under stress that have insufficient ATP resources to execute later apoptotic steps. The rate and mechanisms of cell death in cultures can forecast the destiny of human tissues, particularly when considering chronic diseases. Turning to our results comparing oxygen and MF, Figure 3 isolates the character of the MF from that of oxygen by ignoring the alternate variable in the compilation. An important contrast between oxygen rise and fall, with reasonably similar characteristics for MF rise and fall, suggests different basic lethality mechanisms. In oxygen fall (hypoxia), apoptosis dominated necrosis, opposite to what was observed in the three other cases. This difference between oxygen rise and oxygen fall is not unexpected, considering that human cells have a natural resistance to hypoxia, mediated by hypoxia-inducible factors as reviewed in [18], which upregulate several genes to promote survival in low-oxygen conditions. The similarity in patterns for MF rise and fall, observed here, is a particularity we have reported before in relation to MFs and karyotype measurements [7]. The MF rise, as it impairs proton movement in ATP Synthase, increases the mitochondrial membrane potential (\(\Delta\Phi\)m). If the potential is restored by compensating cellular controls [19], suppression of the field then causes a decrease in the potential. The slight asymmetry between MF rise and fall data (Figure 3), may represent an actual adaptation of the oxidative phosphorylation (OXPHOS) process to the presence of the MFs, and may ultimately lead to uncovering a biological marker for MF exposure. Deviations of less than 3% from the optimal mitochondrial membrane potential (\(\Delta\Phi\)m) of 139 mV result in reduced ATP, and increased ROS [20; 21]. Such a narrow optimal value is not infrequent in physiology, another prominent example in mitochondria being non-heme iron concentration [22]. As OXPHOS is affected by variable EMF levels from the environment over time, mitochondria work more frequently outside their optimal range. Yet, because both consumption of oxygen and MFs are known to induce ROS in reviews [23; 24], the similarity between oxygen rise, MF rise, and MF fall is expected: MFs and oxygen share some common ground in ROS induction. Because 31 out of 36 Transitions are deleterious (\(>\)1 in Table 3), it is also clear that changes in both variables induce physiological stress, by the way of increasing requirements on physiological adaptations. Various Transitions altered necrosis differently (\(\Delta\) = 3.4 in Table 4), but the most Transition-sensitive variables were early apoptosis (\(\Delta\) = 8.7) and the late/early apoptosis ratio (\(\Delta\) = 13.5).