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
Nucleic acid structure determination short lived in solution they need to be generated. This can be done using HO, ascorbic acid, and Fe(II)-EDTA complex which is attached to the backbone through EDTA. The Fe(II) along with ascorbic acid generates hydroxyl radicals which then can react with the nucleic acid molecules. Hydroxyl radical probing is often used in conjunction with chemical probing of nucleic acid molecules that are thought to associate with proteins, this is due to the modification done by hydroxyl radicals. Hydroxyl radicals attack the ribose/deoxyribose ring and this results in breaking of the phosphate backbone, which is independent of secondary structure, as