Abstract
In 1992, senescence marker protein-30 (SMP30) was originally identified as a novel protein in the rat liver. Its physiological functions had not been elucidated for more than a decade until we noticed the amino acid sequence homology between rat SMP30 and bacterial gluconolactonase of Nostoc punctiforme due to a sequence comparison search of GenBank. Our enzymological study revealed that SMP30 catalyzes the hydrolysis of L-gulono-γ-lactone, the reverse reaction of which is the penultimate step in L-ascorbic acid biosynthesis. Moreover, SMP30 knockout mice were found to display the symptoms of scurvy when fed a vitamin C-deficient diet. Using scurvy-prone SMP30 knockout mice like humans, we have performed a series of studies to approach several vitamin C-related problems. Some of the studies allowed us to demonstrate under near in vivo conditions that vitamin C is not essential in carnitine biosynthesis and that it functions to eliminate reactive oxygen species.
