Introduction. For over a century mitochondria were considered to be almost exclusively the source of ATP for the cell. Following the discovery of their genetic system, and their involvement in the control of programmed cell death, there was a drastic change in the way mitochondrial function was viewed. Today the relation between mitochondria and the rest of the cell, the role they play within the context of cell physiology and how they aff ect the pathophysiology of the cell is one of the main challenges facing current research.
Development. The large amounts of oxygen consumed in mitochondria in order to produce ATP make them one of the chief sources of free radicals, as well as their target. Oxidative mitochondrial damage, respiratory chain and ATP defi cits, and infl ammation are the common bases of ageing and of neurodegenerative diseases, and they allow us to use experimental models of ageing, neurodegeneration and sepsis to evaluate both mitochondrial pathophysiology and treatments to prevent it. Recent experimental and clinical data show that melatonin acts as a very powerful antioxidant and anti-infl ammatory agent that is dispersed throughout the whole organism and defends it from oxidative and nitrosative stress.
Conclusions. Experimental models also show that mitochondrial disease is the basis of neurodegenerative disorders and ageing. The capacity of the mitochondria to take up melatonin serves to protect it from the attack of free radicals, thus maintaining its bioenergetic capacity. Melatonin is therefore a mitochondrial homeostatic mechanism that can be used as a pharmacological tool in these situations.