**3. The biological functions of vitamin C**

For a healthy adult, an optimal plasma level of approximately 50 μmol/l is considered sufficient. This ratio may vary based on age, gender, and specific circumstances such as pregnancy or lactation. The Recommended Dietary Allowance (RDA) for vitamin C is 75–90 mg/day for adult men and women [23]. While vitamin C tends to be well-tolerated, adults should not exceed the recommended tolerable upper intake levels, which are set at two grams per day [24]. The most common adverse effects of high-dose vitamin C include gastrointestinal discomforts such as stomach pain and bloating, as well as nausea and diarrhea, particularly when administered in a single oral dose of 5–10 g or daily consumption of 2 g. These symptoms typically subside within 1–2 weeks upon reducing the intake [24].

Vitamin C serves numerous important functions within the body. Its physiological roles are largely associated with the oxidation-reduction properties of vitamin C [13]. L-ascorbic acid plays a crucial role in the synthesis of collagen, which is directly related to scurvy etiology [6]. It acts as an electron donor and serves as a cofactor for certain enzymes involved in collagen, carnitine, neurotransmitter, and amino acid synthesis, particularly for Fe and Cu-containing metalloenzymes like hydroxylases and monooxygenases. Vitamin C, in its reduced form, binds to the active center of iron ions, facilitating the optimal activity of hydroxylases and oxygenases. Additionally, its role as an electron donor contributes to its in vivo antioxidant effect [25–27].

Vitamin C, in addition to its well-known role as an antioxidant, serves various functions in physiological systems of humans and other mammals. It acts as a cofactor in numerous important enzyme reactions, including adrenal steroidogenesis, catecholamine synthesis, carnitine synthesis, collagen synthesis, amino acids, and the synthesis of specific peptide hormones. It has also been reported to be involved in the synthesis of vasopressin released in response to decreased intravascular volume or increased plasma osmolarity [28–30]. Vitamin C acts as a cofactor in biochemical reactions catalyzed by monooxygenases, dioxygenases, and mixed-function oxygenases [31].

Vitamin C, when combined with LDI-glycerol, promotes osteoblast differentiation [32]. It could expedite the healing process by inducing proline and lysine hydroxylation in the collagen triple helix structure [33]. Deficiency in vitamin C, along with deficiencies in folic acid, vitamin B12, and other vitamins, can lead to issues

such as megaloblastic vascular fragility, impaired wound healing, and a weakened immune system [34, 35]. Additionally, vitamin C plays a crucial role in neutralizing free radicals produced at the fracture site [36]. Free radicals disrupt normal cellular activity by affecting body cells and molecules [37]. Vitamin C neutralizes the impact of free radicals, thereby aiding in the reconstruction of damaged cells [38]. Research indicates that vitamin C can enhance the production of genes influencing osteogenesis. For instance, it increases genes like bone morphogenetic protein-2, Runt-related transcription factor 2, and osteocalcin, while decreasing the production of bone-destructive genes such as cathepsin K, tartrate-resistant acid phosphatase, receptor activator of nuclear factor kappa-B, and receptor activator of nuclear factor kappa-B ligand [39]. Considering the positive impact of vitamin C on bone healing, an *in vitro* study utilizing a combination of electrospinning and freeze-drying techniques demonstrated the preparation of highly porous 3D scaffolds comprising different concentrations of vitamin C in poly(lactic acid)/poly(caprolactone)/gelatin (PLA/PCL/Gel). The addition of vitamin C resulted in a decrease in the compressive strength and contact angle of the scaffolds, while enhancing their solubility [40].

Vitamin C stimulates immunity through a range of mechanisms, including macrophage infiltration, cell proliferation, natural killer (NK) cell activity, complement activity, leukocyte phagocytic activity, and the developmental stages of cytokines, including antibody concentrations [41]. Vitamin C has been shown to enhance T-lymphocyte proliferation in response to infection, leading to increased cytokine production and immunoglobulin synthesis [13, 42].

Vitamin C's importance in various stress conditions involving the immune system, including inflammatory processes, has been noted. It is reported to regulate the secretion of proinflammatory cytokines like TNF-α and IL-6. Vitamin C has also been shown to inhibit the production of intercellular adhesion molecules (ICAMs) induced by TNF-α, reducing leukocyte adhesion and secretion, thereby improving microcirculation flow [43–45].

Studies have reported that chronic stress in rats leads to a significant decrease in total leukocytes, lymphocytes, and serum immunoglobulin E (IgE), G (IgG), and M (IgM) levels, and vitamin C supplementation significantly mitigates these effects [46]. It is worth noting that the vitamin C levels in leukocytes, which constitute the cellular composition of the immune system, are many times higher than those in plasma [47].

Vitamin C plays a significant role in maintaining the proper functioning of the antioxidant system in the brain and the nervous system [48]. It has been reported to have a therapeutic effect on memory impairments and neurodegenerative changes and plays a crucial role in neuropathological alterations [49, 50]. Numerous studies have shown that vitamin C modulates the activity of receptors such as glutamate and Gamma-Aminobutyric Acid (GABA) [51–53]. Reports also suggest that vitamin C treatment reduces adverse changes induced by glutamate in immature rat brains [54].

High doses of vitamin C are known to be used in the treatment and prevention of various disorders, including diabetes, cataracts, glaucoma, macular degeneration, atherosclerosis, heart diseases, and cancer [55–63]. The importance of vitamin C supplements is highlighted by the ability to replenish vitamin C levels during various infections [47]. However, it is worth noting that in individuals with severe infections, vitamin C may not confer a survival benefit [64]. At high concentrations, vitamin C acts as a pro-oxidant, selectively targeting and killing cancer cells through the creation of extracellular hydrogen peroxide [65]. It was observed to trigger apoptotic cell death in different carcinomas, including breast cancer, oral squamous cell carcinoma, *Understanding Vitamin C: Comprehensive Examination of Its Biological Significance… DOI: http://dx.doi.org/10.5772/intechopen.114122*

multiple myeloma tumor cells, and pancreatic cancer [66–70]. In a study, high concentrations of vitamin C have been observed to upregulate the expression and activation of p66Shc. Additionally, elevated levels of vitamin C lead to the activation of Rac1 and facilitate apoptotic cell death through the mediation of reactive oxygen species (ROS). Importantly, the activation of Rac1, ROS production, and ensuing cell death induced by vitamin C are dependent on the ser36 phosphorylation of p66Shc. Consequently, the P66Shc/Rac1 pathway emerges as a promising target for vitamin C, presenting potential avenues for exploration in breast cancer therapeutics [66].

It has been reported that high-dose vitamin C can reduce inflammatory reactions, improve oxygen support, and reduce mortality in specific subgroups of critically ill COVID-19 patients and elderly individuals without significant side effects [71]. While antioxidant vitamin supplements are considered safe for physiological systems, many authors have cautioned against high levels of antioxidant vitamins, which can significantly disrupt the physiological balance. It is worth noting that the pro-oxidant effects of ascorbate and other antioxidant vitamins are well recognized by food scientists [72], and these antioxidants may trigger mild oxidative stress due to their pro-oxidant properties [73].
