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If unresolved, ROS accumulation promotes oxidative stress, cellular dysregulation, and subsequent cell death 14

and Naser, S.A., 2016

This is thought to involve both the entry of extracellular Ca2+ via plasma membrane receptor operated Ca2+ channels and the release of Ca2+ from intracellular Ca2+ storages, particularly in the endoplasmicreticulum (calciosome).129 Cytosolic Ca2+ elevation is a major determinant of the oxidative injury.130 As stated above, Ca2+ facilitates mitochondrial permeability transition, a key event leading to both necrosis and apoptosis

(2014b)