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(4) Standard therapy combines atropine, which antagonizes muscarinic receptor overstimulation, with pralidoxime (2-PAM), which reactivates uninhibited or non-aged AChE

277,278,279 When dysfunctional mitochondria cannot be cleared in time by mitophagy, damaged mitochondria accumulate, which results in insufficient energy supply as well as overproduced ROS, thereby triggering intense oxidative stress and cellular damage

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How ROS causes this proliferative effect is best addressed by examining the cellular protective mechanisms that deal with ROS, returning focus to GSH and thiol regulatory pathways