Vitamin C in either the kidney or the liver. In all of the cases where genomic analysis was done on an ascorbic acid auxotroph, the origin of the change was found to be a result of loss-of-function mutations in the gene that codes for L-Gulono-γ-lactone oxidase, the enzyme that catalyzes the last step of the ascorbic acid pathway outlined above. In the case of the simians, it is thought that the loss of the ability to make vitamin C may have occurred much farther back in evolutionary history than the emergence of humans or even apes, since it evidently occurred soon after
Vitamin C -Galactose reacts with the enzyme -galactose dehydrogenase, whereby the lactone ring opens and forms again but with between the carbonyl on C1 and hydroxyl group on the C4, resulting in -galactonolactone. -Galactonolactone then reacts with the mitochondrial flavoenzyme -galactonolactone dehydrogenase. to produce ascorbic acid. -Ascorbic acid has a negative feedback on -galactose dehydrogenase in spinach. Ascorbic acid efflux by embryo of dicots plants is a well-established mechanism of iron reduction, and a step obligatory for iron uptake. All plants synthesize ascorbic acid. Ascorbic acid functions as a cofactor for enzymes involved in photosynthesis, synthesis of plant hormones, as an antioxidant