Why Dysbiosis, SIBO, Hydrogen Sulfide Intolerance, MCAS, and Long COVID May All Be Downstream of a Single Event — The Fenton trap: free iron, lipid peroxidation, and a phospholipid named cardiolipin

When iron-sulfur clusters disintegrate, they don't vanish — they dump their iron into the cell's labile iron pool (the small reservoir of loose, reactive, unbound iron). Loose iron in an inflamed cell is dangerous, because of a piece of chemistry called the Fenton reaction: in the presence of hydrogen peroxide, free ferrous iron generates the hydroxyl radical, the single most reactive and indiscriminate oxidant the body can produce. Hydroxyl radicals don't signal; they simply shred whatever they touch. What they touch, in a mitochondrion, is fat. They initiate lipid peroxidation — a chain reaction that rips through the fatty membranes of the cell. And one membrane fat matters more than any other here: cardiolipin, a phospholipid found almost exclusively in the inner mitochondrial membrane, where it physically organizes the respiratory complexes into efficient supercomplexes. When cardiolipin is oxidized, the electron transport chain loses its scaffolding and its electrons leak even more freely — which makes more superoxide, which makes more peroxynitrite, which damages more iron-sulfur clusters, which releases more iron. If that pattern of iron-driven lipid peroxidation sounds like it has a name, it does — it's the same chemistry underlying ferroptosis, a form of regulated cell death. The colonocyte isn't just running poorly. It is being pushed toward the edge. The takeaway: by