Abstract 2442 Rotenone-induced Complex I inhibition leads to mitochondrial iron accumulation and cytosolic iron depletion

Iron is an essential element in the human body, playing a crucial role in various biological processes, including the electron transport chain (ETC). However, excess iron is toxic and contributes to the development of diseases such as Parkinson's disease (PD). In PD, the first complex of the ETC (Complex I) is deactivated due to sporadic genetic mutations or environmental toxins like rotenone, often accompanied by abnormal iron deposition. We hypothesize that the inhibition of Complex I, which normally contains eight iron-sulfur (Fe-S) clusters, promotes iron accumulation.