Abstract
Alkaptonuria (AKU) is a rare disease characterized by high levels of homogentisic acid (HGA). Although HGA is excreted substantially via urine, AKU patients often suffer from ochronosis, a dark brown pigmentation of joint cartilage, heart valves, and spinal discs, leading subsequently to severe, early osteoarthropathy. A molecular mechanism linking elevated HGA to ochronosis has not yet been found; the chemical identity of the pigment is still not known, nor the mechanism by which pigmentation induces degradation in the physico-mechanical properties of joint cartilage. Here we give key insight on HGA-derived pigment composition and collagen disruption in AKU cartilage. Synthetically derived pigment and pigmented human cartilage tissue both showed hydroquinone-resembling NMR signals, but the previously hypothesized benzoquinone functionality is not observed. EPR spectroscopy showed a radical species in the synthetically derived pigment. Moreover, we observed disruption of collagen triple helix, at the interstrand hydrogen bonds, in pigmented AKU human cartilage. Cartilage from patients with osteoarthritis showed similar disruption. Our results led us to propose a new mechanism for collagen degradation via glycyl radicals, the formation of which is enhanced in AKU due to the redox environment generated by pigmentation.