Role Of Vitamin C In Collagen Formation – Vitamin C (ascorbic acid) plays an important role in maintaining skin health and can promote the differentiation of keratinocytes and reduce melanin synthesis, leading to antioxidant protection against UV-induced photodamage. Normal skin needs high concentrations of vitamin C, which plays many roles in the skin, including the formation of the skin barrier and collagen in the dermis, the ability to counteract skin oxidation and the modulation of cell signaling pathways for cell growth and differentiation. However, vitamin C deficiency can cause or worsen the occurrence and development of certain skin diseases, such as atopic dermatitis (AD) and porphyria cutanea tarda (PCT). Levels of vitamin C in plasma are reduced in AD, and vitamin C deficiency may be one of the factors contributing to the pathogenesis of PCT. On the other hand, high doses of vitamin C significantly reduced cancer cell viability, as well as invasiveness, and induced apoptosis in human malignant melanoma. In this review, we will summarize the effects of vitamin C on four skin diseases (porphyria cutanea tarda, atopic dermatitis, malignant melanoma and herpes zoster, and postherpetic neuralgia) and highlight the potential of vitamin C as a therapeutic strategy to treat these diseases, emphasizing clinical application of vitamin C as an adjunct to medicines or physiotherapy for other skin diseases.

Vitamin C (ascorbic acid, ascorbate) is a simple low-molecular carbohydrate that is essential for the body as a water-soluble vitamin (Lykkesfeldt et al., 2014). As an antioxidant, vitamin C has both oxidized and reduced forms in the body: L-dehydroascorbic and L-ascorbic acid. Although vitamin C is an important antioxidant, humans and other primates obtain vitamin C only from their diet, because they have no ability to synthesize it. With blood circulation to all tissues and organs, concentrations of ascorbic acid in plasma can reach up to 10–160 mM (1–15 mg/ml) after consuming a vitamin C diet, and the excess vitamin can be excreted by the kidneys (Richelle et al. . , 2009). However, there are large differences in the levels of vitamin C in different organs; for example, the brain, liver and skeletal muscle have the highest total content, and that of the testis and thyroid gland is low (Omaye et al., 1987).

Role Of Vitamin C In Collagen Formation

The skin is the largest multifunctional organ on the surface of the human body and consists of three layers: epidermis, dermis and subcutaneous tissue, which form a complete whole with tension and elasticity as the body’s first line of defense against harmful external factors (Hunter, 1973). The epidermis is composed of keratinocytes and dendritic cells, and the stratum corneum can prevent both harmful substances and moisture loss in the skin and is developed from keratinocytes and its lipid matrix (Tagami, 2008); dermis nourishes the skin and is rich in blood vessels and nerve endings (Rittie and Fisher, 2015); and the connective tissue is composed of collagen fibers and elastic fibers in the dermis, which maintain the tension and elasticity of the skin (Carl and Enna, 1979). There is a big difference in the content of vitamin C in the skin’s layers. The content of ascorbic acid in the epidermis is 425% higher than the content in the dermis, and there is a concentration gradient of ascorbic acid in the epidermal keratinocytes (Shindo et al., 1994; Weber et al., 1999).

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It is well known that there are two transport mechanisms for ascorbic acid in the skin, and they depend on sodium ascorbate cotransporter-1 (SVCT1) and sodium ascorbate cotransporter-2 (SVCT2). Dermal fibroblasts present two high-affinity and low-affinity vitamin C transport mechanisms, which may be related to plasma concentrations of ascorbic acid or stress conditions (Butler et al., 1991), showing that skin vitamin C transport properties may be associated with skin healing, antioxidant and antitumor effects. Sodium ascorbate cotransporters (SVCTs), specific sodium-dependent vitamin C transporters, are found in various tissues and organs for vitamin C uptake and transport. SVCT1 is primarily responsible for the transport of epidermal vitamin C, while SVCT2 is responsible for intradermal transport, both of which are shown in Figure 1. SVCT2 in dermal cells (such as fibroblasts) diffuses ascorbic acid transported from the plasma into the epidermis, and SVCT1 in the epidermis delivers ascorbic acid to keratinocytes (Steiling et al., 2007). The SVCT2 transporter in fibroblasts in the dermis transports vitamin C from the blood into the cells (Steiling et al., 2007). If SVCT2 is inside the fibroblasts, it can bind to Mg

But is in a low-affinity state. On the other hand, when SVCT2 is exposed on the fibroblast membrane surface, it can bind to both Mg

In high concentrations of sodium solution and then becomes a high-affinity state and binds to vitamin C (Savini et al., 2008). Vitamin C can be transported into the cell after binding to SVCT1 on the membrane of keratinocytes, and vitamin C and Na

Is reversed on the cell membrane in a 1:2 ratio and then discretely distributed in epidermal keratinocytes (Wang et al., 2000; Steiling et al., 2007; Savini et al., 2008). The expression of SVCT1 mRNA in mouse skin under UVB irradiation showed time- and dose-dependent effects, while SVCT2 mRNA levels did not change significantly, which seems to explain why the antioxidant capacity of the epidermis is greater than that of the dermis (Kang). et al., 2007).

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Vitamin C is involved in the formation of the skin barrier and collagen in the dermis and plays a physiological role in the skin against skin oxidation, in antiaging wrinkles and in cell signaling pathways for cell growth and differentiation, which are related to the occurrence and development of various skin diseases (Ponec et al., 1997b). Vitamin C has a dual role of antioxidation and pro-oxidation, and this role maintains the balance between the two reactions in the body (Kim K. et al., 2015). Ascorbic acid and transition metals, such as Fe

, produce reactive oxygen species (ROS) outside the cell, and high levels of ROS can destroy the antioxidant defense system of cancer cells (Ohno et al., 2009; Conner et al., 2012) because the antioxidant system of tumor cells is incomplete and the balance is broken (Kim K. et al., 2015; Uetaki et al., 2015). High levels of vitamin C in cells lead to oxygen-promoting reactions, which cause DNA damage, depletion of ATP reserves and failure of cellular metabolism (Tian et al., 2014). Vitamin C is also involved in resistance to UV-induced oxidative stress, inhibition of melanogenesis and promotion of keratinocyte differentiation and has been used for a long time as a clinical treatment reagent. Vitamin C deficiency leads to many systemic diseases in humans and causes scurvy in the world’s marines (Carpenter, 2012).

Ultraviolet light, especially UVA, is an important factor that induces oxidative stress on the skin (McArdle et al., 2002). UVA radiation of the skin produces pyrimidine dimers and singlet oxygen in the body. The former weakens the hydrogen bonding effects between DNA double strands. The latter can generate the entire oxygen radical cascade and leads to the alteration of nucleic acids, proteins and lipids, which can induce skin tumors (Lin et al., 2005; Rinnerthaler et al., 2015) There is a sophisticated and complete antioxidant system in the skin, which is used as a defense against the oxidation reaction induced by UV or ozone. The antioxidant system consists of two categories, including the enzyme antioxidant system [superoxide dismutase (SOD) and catalase (CAT)] and the non-enzymatic antioxidant system (vitamin C, vitamin E, and glutathione). Accumulation of ROS across the spectrum of antioxidant defense leads to skin diseases (Godic et al., 2014). However, vitamin C as a supplement has its own instability. Moreover, topical vitamin C supplementation can counteract oxidative stress induced by UVA, which can be assessed in human skin using the chemiluminescence method (Ou-Yang et al., 2004). In addition, the mRNA expression level of matrix metalloproteinase-1 (MMP-1) is significantly increased in the dermal fibroblast after UVA irradiation (Oford et al., 2002). Here, vitamin C can prevent collagen degradation and inhibit the increase of MMP-1, which is the main collagenolytic enzyme responsible for collagen damage in UV-irradiated skin (Oford et al., 2002; Brennan et al., 2003). Moreover, the combination of vitamin E, vitamin C and ferulic acid can reduce the incidence of oxidative stress-induced tumors, and their antioxidant effects are much better than the use of vitamin C alone (Lin et al., 2005).

The synthesis of melanin takes place in the melanocytes in the basal layer of the epidermis and can be transferred to keratinocytes so that melanin is distributed throughout the epidermis (Kwak et al., 2015). Tyrosine and 2-hydroxyphenylalanine (L-dopa) are oxidized to melanin by tyrosinase, which is the rate-limiting enzyme in the entire process (Bin et al., 2014). Whether vitamin C can inhibit melanogenesis is controversial. Most studies have agreed that although it cannot kill melanocytes, vitamin C inhibits melanogenesis; however, some investigators have shown that the role of vitamin C in inhibiting melanogenesis is very weak and cannot inhibit tyrosinase activity (Shimada et al., 2009; Panich et al., 2011). Moreover, the combination of vitamin C and vitamin E inhibits melanocyte production more significantly than vitamin C

What Does Vitamin C Do For Your Skin?

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