Iron is a fundamental co-factor for several cell processes, including oxidative phosphorylation, and mitochondria are the major sites of iron-utilization. Besides being central part of mitochondrial complex I-IV in the electron transport system, iron also regulates the activity of specific enzymes of the citric acid cycle. As a result, mitochondrial iron levels must be tightly regulated, as intracellular iron lack could lead to insufficient energy production, whereas iron overload could trigger ROS (Reactive Oxygen Species) production. However, so far, little information is available on how mitochondrial function is affected by functional and genetic alterations of iron homeostasis; therefore I am aiming at investigating the relevance of mitochondrial iron impairments and the underlying mechanisms.
To access the impact of iron on mitochondrial respiration, I am investigating mitochondrial activity and ROS production mainly by means of high resolution respirometry (OROBOROS Instruments, Austria) and immunofluorescence techniques.
Our ongoing experiments indicate that mitochondrial function testing can be successfully performed in mouse tissues. Analyses of liver samples indicate that dietary iron supplementation triggers changes in oxidative phosphorylation, and has a direct impact on the activity of the electron transfer system complexes.
