What effect does increased calcium ion concentration due to dysfunctional Ca-ATPase have on the cell?

Increased calcium ion concentration within a cell can lead to significant alterations in cellular function, particularly when there is a dysfunction in the Ca-ATPase, an enzyme responsible for transporting calcium out of the cell. When levels of intracellular calcium rise excessively, a cascade of intracellular events is triggered, notably the activation of pro-apoptotic enzymes.

High intracellular calcium levels disrupt the normal signaling pathways and can lead to cellular injury and apoptosis (programmed cell death). This is largely due to calcium's role as a signaling molecule; elevated levels can activate various enzymes, including those involved in the apoptotic pathway, such as calpains and caspases. These enzymes can initiate the processes that lead to cell death, thereby underscoring the link between dysfunctional calcium handling and apoptosis.

In contrast, decreased cell membrane permeability does not typically result from increased calcium; rather, alterations in permeability are more related to other factors. The stimulation of ATP production is generally a response to increased demand rather than a direct consequence of calcium elevation, and high calcium levels do not promote cellular repair processes—instead, they often contribute to dysfunction and cell death. Therefore, the activation of pro-apoptotic enzymes appropriately describes the pathological effect of increased intracellular calcium due to dysfunctional Ca-ATPase