**2. Vitamin C and scurvy**

What is vitamin C, and where does this odd name come from? To answer this question we have to go back to the work of Kazimierz Funk, a pioneer biochemist who studied the etiology of some "deficiency disorders" caused by the lack of key nutritional factors [6]. Funk hypothesized that each of those disorders is due to a diet deficient in a specific "vital amine". In 1912, Funk named each of those (still hypothetical) factors after the first letters of the alphabet. Vital amines changed their name in vitamines and then vitamins, when it was clear enough that, with the exception of a few belonging to the B complex, they are not amines. In Funk's nomenclature, vitamin C is the one preventing the disease known as scurvy. Of course, Funk had no idea of the chemical nature of the factor. He only suggested that a deficiency in this unknown molecule caused the disease, and, conversely, the uptake of vitamin C could cure the disease. Over the centuries scurvy has killed millions, and especially sailors in the long voyages of exploration that occurred between the late XV and mid-XIX centuries [7]. Scurvy causes a variety of symptoms, which hardly seem to relate (**Figure 1**).

Interestingly, the symptoms appear progressively, the first one being usually lethargy, followed by neurological disorders and impaired vision. Subsequent signs of the disease include bleeding, spots, swelling gums, bone fractures, problems in wound healing, and even old scars and fractures re-open and re-break [8]. The identification of the anti-scurvy factor by Szent-Györgyi opened the way to a new line of research, aimed at understanding not only the pathogenesis of scurvy but also the mechanisms by which AsA can prevent and cure it. It took, however, almost three decades before the riddle of the biochemical function of AsA could be, at least in part, solved.

It is worth mentioning that most animals do not need AsA supplementation in their diet, because they can produce it by means of a well-characterized biosynthetic pathway [9]. Humans and a few other mammals, as well as some birds and fishes, have lost the capability to synthesize AsA because of the loss of function of the gene coding for the terminal enzyme in the pathway, l-gulono-1,4-lactone oxidase (GULO) [10]. This is the cause of our dependency on external AsA sources (mostly plant-derived food, and primarily fleshy fruits) for our survival.

What is the function of AsA in cell metabolism? A classical reverse genetic approach, frequently used when trying to identify the function of a gene or metabolite, is based on the knocking out of that gene (or of a gene regulating the biosynthesis of the metabolite of interest) and the characterization of the resulting phenotype [11]. In the case of AsA, we do not have to look too far to find the perfect experimental model: all organisms, including humans, who are unable to synthesize AsA are

*The Function of Ascorbic Acid through Occam's Razor: What We Know, What We Presume… DOI: http://dx.doi.org/10.5772/intechopen.109434*

**Figure 1.** *Partial list of scurvy-related symptoms.*

knockout mutants in the *GULO* gene, and the resulting phenotype is clear and known for centuries. This phenotype is scurvy.
