Reactive oxygen species (ROS) are a molecular group that can be produced in the course of different physiological processes and react with a large variety of oxidizable cellular components, therefore, oxidation-reduction (red-ox) reactions involving ROS have gained attention as important chemical processes with implications in cellular signal transduction.

Mitochondria are probably the most important source of increased free radical production and thus have a crucial role in generation oxidative stress. Additionally, mitochondria are one of the possible targets by which oxidative stress exerts its effects on cellular deterioration. Nowadays,  the involvement of this organelle in patho-physiological processes and its relation to oxidative stress is being clarified.

ROS are able to increase cytosolic free Ca²⁺ concentration ([Ca²⁺]_c) and have been considered as pathogenic factors in different tissues and cells, including the exocrine pancreas. An increase in [Ca²⁺]_c due to disturbance of Ca²⁺ homeostasis by ROS can cause morphological and functional alterations of the cell, hence it has been clearly established its contribution to disease and cell death.

The effect of secretagogues on mitochondrial activity and cellular oxidative state, as well as the effect of ROS on Ca²⁺ signalling, enzyme secretion and mitochondrial activity in the exocrine pancreas  will be discussed in the present mini-review.