From Arndt von Hippel
Steve Benner’s group at the University of Florida, Gainesville, plans to reconstruct ancient versions of mammalian uricase in order to determine why humans retain high uric acid levels in their blood (23 April, p 44). They wonder if reducing uric acid levels by treatments for gout or hypertension might have adverse side-effects.
Lubert Stryer once proposed that our high blood uric acid levels replaced vitamin C’s antioxidant effect and protected our cellular DNA from oxidative damage – for unlike elephants and other long-lived mammals, primates long ago lost their ability to regenerate vitamin C. He pointed out that lower primates with far lower blood uric acid levels had comparatively short life spans and high cancer rates.
Furthermore, a recent Nature report suggests that the near-saturation levels of uric acid within human cells means significant leakage of intracellular fluid can promote uric acid crystal formation in tissue fluids. Thus uric acid crystallisation signals tissue damage in humans, and uric acid crystals (but not dissolved uric acid) serve to initiate inflammation and encourage immune cells to attack microbes whose proteins appear in synchrony with cell damage. Uric acid crystals may even underlie some cases of chronic inflammation and autoimmunity in genetically susceptible individuals.
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