**1. Introduction**

Several reports have pointed towards a putative link between vitamin C (vitC) deficiency and lifestyle-associated disease [1–6]. Moreover, vitC deficiency has also been associated with impaired brain development and reduced hippocampal function in experimental animal studies [7–10]. Scurvy is the terminal outcome of a prolonged period of severe vitC deficiency (a plasma concentration <11 μM [11]) and is rarely encountered, as it can be prevented with as little as 10 mg vitC/day.

In contrast, marginal vitamin deficiency or hypovitaminosis C, defined as a plasma concentration below 23 μM [11], has been estimated to affect as much as 10% of adults in the industrialized world [12–14], with subgroups, such as smokers and families with a low socio-economic status, displaying an even higher prevalence [15–19]. Adverse effects of marginal vitC deficiency could, therefore, potentially affect a substantial amount of people who, unknowingly and devoid of known clinical symptoms, are at risk of experiencing negative long-term effects of vitC deficiency, including increased mortality associated with a variety of disease complexes [20].

The pharmacokinetics of vitC, *i.e.*, the absorption, distribution, metabolism and elimination, is quite complex and involves several different active and passive transport mechanisms, as well as intracellular reduction permitting the recycling of vitC within specific tissues [18,21]. Furthermore, vitC is differentially distributed between tissues, with brain and neurons, in particular, upholding a much higher concentration than most other organs [22–24]. However, whereas vitC homeostasis has been studied in detail during sufficiency [25–28], less is known about the potential adaptive mechanisms during deficiency. Thus, for example, studies of vitC transport activity during deficiency have not provided evidence supporting a direct relationship between local tissue-concentration and the expression of vitC specific transporters [29–31], prompting suggestions of possible alternative transport mechanisms [29]. The present review elaborates on the mechanisms currently known to be involved in the regulation of vitC transport and the potential effects during states of deficiency.
