Vitamin C plays a vital role in the perioperative period by enhancing immune function, supporting tissue growth and repair, and protecting the brain. It is crucial for collagen formation, reducing oxidative stress, and maintaining cognitive health. Adequate levels of vitamin C are essential for surgical recovery and reducing complications.

Mechanisms of Action and Benefits:

• Immune Function and Inflammation Control: Vitamin C is highly concentrated in white blood cells and mitigates oxidative damage in areas of infection, thus decreasing host cell injury. It promotes T-cell proliferation and enhances chemotaxis while downregulating pro-inflammatory cytokines such as IL-2, IL-6, and TNF-alpha via NF-kappaB. (11,12)
• Antioxidant Properties and Neuroprotection: As a potent antioxidant, vitamin C scavenges free radicals like superoxide, reducing oxidative stress that contributes to neurodegenerative diseases. It protects the brain against oxidative damage, decreases the impact of ischemic strokes, and supports cognitive function. (1,4,7)
• Collagen Synthesis and Wound Healing: Vitamin C facilitates the hydroxylation of proline and lysine residues in collagen, allowing for the proper folding and maturation of collagen necessary for wound healing. It supports tissue repair processes, helping improve postoperative recovery. (1)
• Neurotransmitter Modulation: Vitamin C functions as a neuromodulator of neurotransmitter systems, including glutamatergic, dopaminergic, cholinergic, and GABAergic transmission. It regulates acetylcholine and catecholamine release, essential for memory and learning. (7,8,9)
• Support for Hypoxic Conditions: Vitamin C assists in the hydroxylation of hypoxia-inducible factor 1α (HIF-1α), enabling cells to respond to low oxygen levels by activating genes involved in glycolysis, angiogenesis, and cell survival. This role is particularly important during surgical stress and recovery. (2)
• Interaction with Other Antioxidants: In aqueous compartments, vitamin C can recycle alpha-tocopherol (vitamin E) by reducing the alpha-tocopheroxyl radical back to its active form, enhancing antioxidant defense in lipid-rich environments such as the brain and cell membranes. (5,6)

References

1. Harrison FE, May JM. Vitamin C function in the brain: vital role of the ascorbate transporter SVCT2. Free Radic Biol Med. 2009;46(6):719-730. doi:10.1016/j.freeradbiomed.2008.12.018
2. Semenza GL. HIF-1, O(2), and the 3 PHDs: how animal cells signal hypoxia to the nucleus. Cell. 2001;107:1–3.
3. Rice ME, Russo-Menna I. Differential compartmentalization of brain ascorbate and glutathione between neurons and glia. Neuroscience. 1998;82:1213–1223.
4. Jackson TS, Xu AM, Vita JA, Keaney JF., Jr Ascorbate prevents the interaction of superoxide and nitric oxide only at very high physiological concentrations. Circ Res. 1998;83:916–922.
5. Niki E, Noguchi N, Tsuchihashi H, Gotoh N. Interaction among vitamin C, vitamin E, and β-carotene. Am J Clin Nutr. 1995;62(Suppl):1322S–1326S.
6. May JM, Qu ZC, Mendiratta S. Protection and recycling of α-tocopherol in human erythrocytes by intracellular ascorbic acid. Arch Biochem Biophys. 1998;349:281–289.
7. Sandstrom MI, Rebec GV. Extracellular ascorbate modulates glutamate dynamics: role of behavioral activation. BMC Neurosci. 2007;8:32.
8. Kuo CH, Hata F, Yoshida H, Yamatodani A, Wada H. Effect of ascorbic acid on release of acetylcholine from synaptic vesicles and release of noradrenaline from synaptic vesicles in rat brain. Life Sci. 1979;24:911–915.
9. Sam C, Bordoni B. Physiology, Acetylcholine. [Updated 2023 Apr 10]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-.
10. Maxfield L, Crane JS. Vitamin C Deficiency. (Updated 2021 Jul 18). In: StatPearls [Internet]; 2021 Jan-.
11. Manning J, Mitchell B, Appadurai DA, et al. Vitamin C promotes maturation of T-cells. Antioxid Redox Signal. 2013;19(17):2054-2067. doi:10.1089/ars.2012.4988
12. Gęgotek A, Skrzydlewska E. Antioxidative and Anti-Inflammatory Activity of Ascorbic Acid. Antioxidants (Basel). 2022;11(10):1993. doi:10.3390/antiox11101993