The effect of aluminum on mitochondrial dysfunctions

Aluminum is the most widely distributed metal in the environment and is extensively used in daily life, although it has no known biological functions. Its pro-oxidant activity, along with its ability to mimicry essential metals, elicits oxidative stress and mitochondrial dysfunction that culminate in apoptosis. Remarkably, aluminum affects iron-sulfur cluster proteins and antioxidant enzymes, triggering a cascade of events that contribute to adenosine triphosphate depletion and requiring the cell to shift the metabolism to mitigate its deficiency. Disturbances in cell homeostasis are then expressed as biochemical and histological alterations in several organs. For instance, tissue damage induced by aluminum can lead to liver and heart dysfunction as well as neurodegenerative diseases, such as Alzheimer's and Parkinson's diseases. Therefore this chapter aims to provide a broader view of the mechanism of aluminum toxicity in cell metabolism with the mitochondria as a target organelle, with a focus on tissues with high energy requirements.