The hypothesis that is proposed is that tyrosinase, an enzyme widely found 
within the human body is implicated in the ochronosis that occurs in 
alkaptonuria; an autosomal recessive condition first used by Archibald Garrod to 
describe the theory of "Inborn Errors of Metabolism." The disease results from 
the absence of a single enzyme in the liver that breaks down homogentisic acid; 
this molecule becomes systemically elevated in sufferers. The condition is 
characterised by a clinical triad of symptoms; homogentisic aciduria from birth, 
ochronosis (darkening) of collagenous tissues (from ∼30years of age) and 
ochronotic osteoarthropathy in weight bearing joints due to long term ochronosis 
in them (from ∼40years of age). Tyrosinase, a polyphenol oxidase has been shown 
in many species to contribute to the darkening of tissues in many organisms; 
including humans in the production of melanin. Tyrosinase under the right 
conditions shows alterations in its substrate specificity and may contribute to 
the darkening seen in AKU where it moves away from polymerising tyrosine but 
also homogentisic acid, the causative molecule in alkaptonuria, that is present 
in excess.