Iron is essential for complex IV in the electron transport chain. Iron-heme centres work together with copper centres to reduce oxygen to water and generate ATP. If there is insufficient bioavailable iron or copper, oxygen utilization and ATP production go down. But excess free iron is one of the most potent generators of hydroxyl radicals via Fenton chemistry. This stuff will wreck mitochondrial membranes and mtDNA = higher heteroplasmy rate. So you need iron for energy production, but too much unbound or poorly handled iron is a major problem. The body manages this through ferritin, transferrin, copper‑dependent ferroxidases like ceruloplasmin ( (which needs copper and B6) and hephaestin, and the hepcidin-ferroportin axis that regulates iron absorption and release. This is why iron is never just about iron; it is about the whole network of nutrients, hormones, and proteins that handle it. Low ferritin with high transferrin saturation tells a completely different story than low ferritin with low saturation, and low ceruloplasmin often points to a copper issue that secondarily disrupts iron metabolism rather than primary iron deficiency. Testing matters and its important to do complete iron panels (ferritin, serum iron, transferrin/TSAT, CRP, and sometimes ceruloplasmin and copper) to actually try to figure out what's going on.