It is no longer doubted that calcium functions as a second messenger in animals and plants. This is only possible because cells maintain cytosolic calcium concentrations many orders of magnitude below that of extracellular or organelle calcium. Environmental stimuli are perceived by receptor proteins which trigger transient elevation of cytosolic calcium using internal or external sources. The spatial and temporal distribution and the magnitude of calcium elevation determines the specific cellular response at the molecular level (Cheek 1991). The fine balance of cytosolic calcium homeostasis in animal cells is highly sensitive to oxidising conditions (Duncan 1991). Elevated cytosolic calcium resulting from oxidative perturbation of calcium homeostasis is believed to be responsible for the subsequent cellular injury and death (Nicotera et al. 1991). Transient stimulation of cytosolic calcium in sublethal oxidative stress may be a mechanism by which oxidative attack is perceived by the animal cell (Nicotera et al. 1991). Our understanding of oxidative stress and plant responses to it would be greatly advanced if it can be shown that similar processes occur in plant cells. This paper briefly presents the mechanism of oxidative disruption of calcium homeostasis in animal cells and summarises the evidence that the same scenario applies to plants.
Dynasore protects ocular surface mucosal epithelia subjected to oxidative stress by maintaining UPR and calcium homeostasis