Open access peer-reviewed chapter
Abstract
The topical use of vitamin C as a cosmetic arouses much interest within the field of medicine and cosmetic dermatology. Its different forms of presentation have evolved over the years to increase its bioavailability. Its use in cosmetics generates significant amounts of money day after day. Is there scientific evidence of its usefulness and its absorption? Is there scientific support for the marketing campaigns on the cosmetic use of Vitamin C? Does it present any contraindication or can it be used universally? What is new in the topical use of Vitamin C? Are all cosmetic presentations effective? Is it as useful as the cosmetic industry tells us?
Keywords
- vitamin C
- cosmetic use
- antiaging
- antioxidant
- depigmenting
- effectiveness
1. Introduction
The role of ascorbic acid or vitamin C (water-soluble vitamin) in skin health is well known, as we will see later, as early as the eighteenth century its deficit or lack was associated with different skin-type pathologies.
In this chapter, the author, based on the definition of cosmetic products and their economic importance, makes a basic description of the aging process, as well as the anatomy of normal skin and aged skin as an essential basis for understanding the rest of the chapter.
The following sections develop the role of vitamin C in skin health, as well as the different clinical conditions in which it has been shown to be effectively used topically. It includes biochemical bases that allow us to understand, in a simple and practical way, the mechanisms of transport of vitamin C through the different layers of the skin, as well as which are the most effective cosmetic forms that favor its skin absorption.
2. Definition of cosmetic
The Federal Food, Drug, and Cosmetic Act (FD&C Act) defines cosmetics by their intended use, as “articles intended to be rubbed, poured, sprinkled, or sprayed on, introduced into, or otherwise applied to the human body…for cleansing, beautifying, promoting attractiveness, or altering the appearance” [FD&C Act, Section 201(i)]. Among the products included in this definition are skin moisturizers, perfumes, lipsticks, fingernail polishes, eye and facial makeup preparations, cleansing shampoos, permanent waves, hair colors, and deodorants, as well as any substance intended for use as a component of a cosmetic product [1].
3. Cosmetic products economic impact
Physical beauty is a concept that varies according to the time humanity is living, and archaeology shows us that the human being has always felt the concern to care for and maintain their skin and body
The year 1905 saw the opening of Elizabeth Arden’s first beauty salon in Melbourne, with L’Oreal, Max Factor, Maybelline, and Helena Rubinstein as its main rivals. The cosmetics industry was favored by the research and discovery of new chemical principles that were used especially for the facial beautification [2].
According to the latest forecasts, the total revenue of the global cosmetics market will reach the figure of 93.8 billion dollars in 2022. Facial cosmetics continue to rank third in the ranking of products that generate the most revenue in the global cosmetics market, representing 17.6% of the total income of this industry in 2022 [3].
In Spain, the cosmetics industry generates 250,000 indirect jobs [4]. The economic impact of this business sector is undeniable; hence, the cosmetics industry and the scientific community are immersed in a continuous search and study of new active ingredients and formulations that can respond to this market demand.
4. Skin ageing
Aging is a physiological process that involves the progressive accumulation of changes associated with the passage of time, being responsible for the increased susceptibility to disease and death that accompanies advanced age [5].
Skin aging is particularly important due to its social impact. It is visible and also represents a model organism in which to investigate the aging process. The so-called “biological clock” affects both the skin and the internal organ system in a similar way [6].
We can refer to an intrinsic aging, especially directed by our genome, and an extrinsic aging, determined by a large number of factors, included within the concept of exposome [6].
The term “exposome” was coined in 2005, by the American epidemiologist Christopher Wild, and describes the totality of the exposures to which an individual is subjected from conception to death. It includes both external and internal factors as well as the human body’s response to these factors [7].
Skin aging consists of external and internal elements and their different interactions, which as we have said above affect the human being from the moment of conception to death, as well as the human body’s response to these factors. As a result of this conjunction, biological and clinical signs of skin aging will appear [6, 7].
The environmental factors that configure the exposome in skin aging are divided into the following categories (Figure 1).
Solar radiation: UV, visible light, and infrared.
Air pollution.
Tobacco.
Nutrition.
Miscellaneous: lack of sleep, stress, temperature.
Cosmetic products.
Figure 1.
The human exposome. Image by the author.
5. Normal skin structure
The skin is the largest organ of the human body and performs the following functions:
Barrier function between our body and the outside.
Protective function against mechanical damage, radiation microorganisms, and toxic agents.
Regulation of body temperature.
Homeostasis of body water.
The skin is organized into three layers: epidermis, dermis, and hypodermis.
5.1 Epidermis
It consists of a layer of stratified squamous epithelium that is in continuous renewal. It presents different cell types: keratinocytes (95%), melanocytes, Langerhans cells (immune function), and Merkel cells (transmitters of mechanical stimuli). The epidermis is an avascular layer.
The keratinocyte moves from the basal membrane to the surface of the skin, forming different epidermal layers with different morphologies: basal or germinative stratum, lucidum stratum, spinosum stratum, granular stratum, and corneum stratum. Among other functions, epidermis prevents moisture loss from the skin (Figure 2) [8].
Figure 2.
Anatomy of the epidermis. Image taken from:
5.2 Dermis
It is divided into two different regions: the upper papillary dermis and the lower reticular dermis. The papillary dermis is located just below the dermo-epidermal junction and has conical forms called dermal papillae, and these dermal papillae interdigitate with the network of epidermal crests, increasing the interface between dermis and epidermis.
The dermis is made up, especially, of blood vessels and nerve endings. Type I and III collagen fibers, fibroblasts, fibrocytes, fibroblasts, and elastic fibers, which maintain the tension and elasticity of the skin. It also contains the sweat glands and the base of the pilosebaceous system [8].
5.3 Hypodermis or subcutaneous tissue
Hypodermis or subcutaneous tissue is the deepest layer of the skin; it is located below the dermis and above the muscle. Adipocytes that are arranged in lobes separated by septa of connective tissue predominate in their cell population (Figure 3) [8].
Figure 3.
Layers of the skin. Image taken from:
6. Structure of aged skin
The process of skin aging results in the following histological changes.
Thinning of the epidermis.
Decreased proliferation of keratinocytes.
Decrease in cellular renewal.
Flattening of the dermo-epidermal union
Decreased surface contact between epidermis and dermis.
Atrophy of the dermis.
Reduction in the number and functionality of fibroblasts.
Atrophy of fat tissue by lipolysis plus atrophy of muscle mass.
The total of these various changes causes an increase in the fragility of the skin, a decrease in the exchange of nutrients between the dermis and the epidermis (avascular layer), and alterations in the healing process. It also decreases the number and diameter of collagen fiber bundles, appears a disorganized collagen, and increases the proportion of collagen type III versus collagen type I.
There is a general thinning of the skin and a weakening of its adipose-muscular support to which the physiological bone resorption that appears in the aging process must be added. This loss of skin tissue, especially dermal and hypodermic, favors the appearance of visible signs of aging, such as wrinkles [9].
7. Vitamin C and skin
The skin is not a simple covering of the body but rather a multifunctional organ, the largest in our body, and its appearance generally reflects the health and functional efficiency of its underlying structures.
Its continuous contact with the outside makes it the most attacked organ in our body and the first to show signs of aging [10].
7.1 Role of vitamin C in the health and functionality of the skin
It is easy to deduce how important is the skin and the need to keep it in a healthy state, nutrition plays a very important role in this health since as we will see later, the human body is unable to synthesize vitamin C so an adequate exogenous supply is needed.
Certain nutritional alterations affect the integrity of the skin as well as its main biological functions.
In the specific case of vitamin C, we know that its presence in the body at adequate concentrations is vital for the growth and maintenance of bone health, dental, gums, ligaments, and blood vessels, and in the process of collagen synthesis.
Vitamin C is present in the body in two forms: L-ascorbic acid (reduced form) and L-dehydroascorbic acid (oxidized form). As a result of a mutation in the gene-encoding L-gulonolactone oxidase, an enzyme required for the synthesis of vitamin C, man, and other primates is unable to synthesize this vitamin, requiring an exogenous supply.
The pioneer in the study of vitamin C and the pathologies associated with its deficiency, as well as its clinical and cutaneous manifestations, was Dr. James Lind in his Treatise on Scurvy (1753) [11]. We can also find other research that has been carried out on skin disorders and abnormalities due to vitamin deficiencies and their correction with oral or topical supplementation [12].
The content of vitamin C in the skin is highly variable, being 425% higher in the epidermis than in the dermis, although these figures vary depending on the studies reviewed, possibly influenced by the difficulty of handling the samples and the area studied, and donor age. In turn, we found that there is a concentration gradient of ascorbic acid in the keratinocytes of the epidermis. The lowest concentration of vitamin C is found in the most superficial part of the epidermis, while the highest is found in the deeper layers, possibly due to the depletion of the most superficial cells by their continued exposure to the environment [12, 13].
We also know that vitamin C levels are lower in people who are photoaged or who suffer any degree of skin damage due to continuous exposure to the sun. Sun exposure, among other factors, generates reactive oxygen species (ROS), such as superoxide anion and hydrogen peroxide, against this increase in ROS, the body sets, in motion, a series of endogenous antioxidant mechanisms to try to neutralize them, and we refer to oxidative stress when these endogenous mechanisms are unable to completely neutralize ROS. This oxidative stress can produce changes in the genetic load of the individual and it has been observed that excessive exposure to oxidative stress caused by UV radiation or environmental pollution is associated with a reduction in levels of vitamin C present in the epidermis [13].
7.2 Bioavailability and absorption of vitamin C in the skin
In order to perform its functions, ascorbic acid must be actively transported into the cell, a task performed by specific transporters present in the cell membrane.
In humans, two transporter families capable of transporting vitamin C have been described [14].
The first one corresponds to glucose transporters or GLUTs, and within this group, isoforms 1,2,3,4, and 6 have been described that act as dehydroascorbic acid transporters.
The second is a family of transporters that take advantage of the electrochemical gradient of the Na + cation to transport ascorbic acid, which is known as SVCTs (sodium-ascorbate cotransporter). Two functional isoforms are described: sodium-ascorbate cotransporter-1 (SVCT1) and sodium-ascorbate cotransporter-2 (SVCT2).
Sodium-dependent vitamin C transporters (SVTCs) are responsible for the absorption of vitamin C and its transport through the skin layers [14]. These two transporters are present in various tissues and organs.
SVCT1 is the main one in charge of transporting vitamin C at the epidermal level, while SVCT2 is in charge of taking vitamin C to the dermis, to transfer it, especially to the fibroblasts. From the dermis, vitamin C is transported to the epidermis where SVCT1 is responsible for providing ascorbic acid to the keratinocytes [15].
The specific location of SVCT1 in the epidermis is of great importance since it is an avascular layer and suggests that the combined expression of both transporters 1 and 2 ensures the effective absorption and intracellular accumulation of vitamin C and informs us of the high dependence on vitamin C of this tissue [13].
SVCT1 has a low affinity for vitamin C but has a high transport capacity; in contrast, SVCT2 found in almost all cells of the body has a high affinity for vitamin C but a low transport capacity [16, 17].
It seems likely that, as occurs in other tissues, the levels of vitamin C in the skin respond to increases in its plasma concentration, especially with intakes that exceed the recommended daily amount. However, some authors suggest that skin levels do not increase once plasma saturation has been reached, so nutritional supplementation with vitamin C would be effective in raising skin vitamin C levels, only in people whose levels plasma are below the saturation point (Figure 4) [18].
Figure 4.
Distribution of vitamin C in the skin mediated by SVCT1 and SVCT2. The black arrows indicate the transport from the dermis to the epidermis (avascular layer). Image taken from:
8. Mechanisms of production of skin photodamage
In a previous section, we discussed the importance of the exposome and one of its factors, sun exposure, which is closely linked to the skin photoaging process [7]. This photodamage is favored by the presence of trans-urocanic acid, a by-product of the epidermal protein filaggrin that is present in the skin and acts as a chromophore for solar radiation photons [19].
Excess sun exposure induces oxidative stress that can produce changes in the genetic load of people.
UVB rays (290–320 nm) directly damage DNA, while UVA rays (320–400 nm) produce mutations indirectly by generating reactive oxygen species (ROS). UV radiation is associated with aging and the appearance of skin cancer [20] by acting as a trigger for important pro-inflammatory processes.
How does ROS act in the skin aging process?
Activating cell receptors for pro-inflammatory cytokines: interleukin-1 (IL-1β), IL-6, IL-8, and tumor necrosis factor-alpha (TNF-α), among others.
Inducing the activation of protein transcription factor 1 (AP-1), which activates matrix metalloproteinase enzymes (MMPs) that degrade collagen type I and III, while blocking the synthesis of pro-collagen I and III by inhibiting transforming growth factor beta (TGF-β) receptor signaling.
MMPs are proteolytic enzymes that are responsible for remodeling the extracellular matrix and that together can degrade all its constituents [21]. UV radiation triggers the production of pro-inflammatory cytokines that favor the expression of MMP-1, MMP-3, MMP-9, and MMP-12, which, as we have seen, accelerate the degradation of collagen, and favor the accumulation of elastin, generating manifestations of some signs of photoaging such as hyperpigmentation, telangiectasias, coarse skin texture, deep wrinkles, and solar elastosis [20, 22]. As MMPs also promote angiogenesis as a result of this stimulation, they favor cancer cell growth and spread (Figure 5) [23].
Figure 5.
Scheme of the mechanisms of photodamage production on the skin mediated by ROS. Image is taken from Altobelli, G.G. et al. (2020) “Copper/zinc superoxide dismutase in human skin: Current knowledge,” Frontiers in medicine, 7. Available from:
9. Formulating vitamin C for topical/cosmetic use
There are numerous studies that support and justify the topical/cosmetic use of vitamin C. Among its actions, we can highlight its ability to eliminate ROS, its action as a cofactor for the enzymes prolyl and lysyl hydroxylase, responsible for the stabilization and cross-linking of synthesized collagen by fibroblasts, the stimulation of collagen synthesis directly by activation of messenger ribonucleic acid (mRNA) and the preservation of collagen in the skin by regulating the enzymes responsible for its degradation [19].
Oral vitamin C supplementation is less effective than topical, as its absorption is limited by intestinal transport mechanisms, so the topical route is the one of choice when we want to increase the concentration of vitamin C in the skin [24].
Vitamin C in its active form L-ascorbic acid is hydrophilic (water-soluble) and very unstable, and this characteristic conditions its skin absorption due to the hydrophobic nature of the stratum corneum. The first preparations of vitamin C for topical use presented the problem of its rapid oxidation of ascorbic acid in dehydroascorbic acid on contact with air and metals or if they were preserved at high temperatures.
For a good penetration through the epidermis, several studies report that the optimal pH of the preparation has to be less than 3.5, and this pH is achieved with the addition of ferulic acid that acts as a stabilizer of the L-ascorbic acid molecule.
Different strategies have been tested to solve the problem of the stability of vitamin C, such as encapsulation, formulation at low pH, oxygen-tight packaging, and the addition of electrolytes and other antioxidants [25].
The optimal concentration will depend on the type of formulation and presentation but should always be greater than 8% and less than 20%, higher concentrations have been irritating and have not offered an increase in their activity, and may be formulated alone or associated with other active ingredients [26].
The cosmetic industry has sought greater stability and easier formulation with derivatives such as ascorbyl 6 palmitate, magnesium ascorbyl phosphate, sodium ascorbyl phosphate, ascorbyl 2-glucoside, ascorbyl 2-phosphate6-palmitate, and 3-O-ethyl ascorbate [26].
Among the nonsaline derivatives of ascorbic acid used in formulations intended for topical use, we highlight:
Ascorbyl 2-glucoside is important for its great stability against oxidation and high temperatures, as well as its ease of formulation.
Ascorbyl 6 palmitate is very stable in cosmetic formulas at neutral pH and effective against burns produced by UV radiation with reduced redness and antioxidant and anti-inflammatory effects.
Ascorbyl 2-phosphate is usually formulated as sodium and magnesium salts. Stable at pH 7.0, its effectiveness depends on its conversion
in vivo into ascorbic acid.Magnesium-L-ascorbyl-2-phosphate is the most stable of ascorbic acid derivatives, protects against UVB radiation, has been evidenced by its penetration through the epidermis forming ascorbic acid by dephosphorylation of membrane cells, and is a good scavenger of free radicals and stimulates collagen synthesis [20].
Ascorbyl 2-phosphate 6-palmitate can penetrate through the skin and become ascorbic acid.
3-O-ethyl ascorbate is more lipophilic than ascorbyl 2-glucoside, which promotes its penetration through cell membranes [26].
The search for improvement in activity and skin penetration of vitamin C on the skin has led to clinical studies using the DNA aptamer: “Aptamin C”. Studies such as that of Choi, S. et al. demonstrate the effectiveness
10. Vitamin C actions on the skin
10.1 Antioxidant against photodamage caused by UV rays
Vitamin C has different mechanisms of action as an antioxidant substance listed below.
It neutralizes the free radicals present in the aqueous compartment of the cell by a process of donation and transfer of electrons, this donation occurs sequentially, after donating the first electron is formed a more stable free radical that is ascorbate, and after donating the second electron it is transformed into dehydroascorbic acid. Dehydroascorbic acid can be enzymatically converted back to L-ascorbic acid or broken down [24].
It is an essential cofactor in a large number of enzymatic reactions.
It inhibits the action of protein transcription factor-1 (aP1) (see paragraph 8), acting vitamin C as a regulator of the MMP, and, therefore, decreasing the damage that these MMPs produce to collagen fibers [18, 19, 20, 21, 22, 23].
Reduces inflammation and immunosuppression induced by UV rays as it prevents reduction of Cd1a (as we saw in paragraph 8), this Cd1a is an antigen-presenting molecule that is intensely expressed in Langerhans cells and whose immunoprotection function decreases with exposure to UV irradiation [29].
It enhances efficiency and protection against UV damage when added to products intended for use as sunscreen (Figure 6) [30].
Figure 6.
Mechanisms of action of vitamin C onto the ROS and its effect on skin damaged by UV radiation. Image by the author.
10.2 Depigmenting
We understand by melanogenesis the process that leads to the production of the pigment melanin from melanocytes. The melanoblasts, precursor cells of the melanocytes, are preferably located in the basal layer of the epidermis and in the hair follicles [31].
The melanocytes of the skin are surrounded by keratinocytes in a ratio of one melanocyte to approximately 36 keratinocytes, and the melanocytes transfer the melanin they synthesize to the keratinocytes.
Melanogenesis is influenced by:
genetic factors such as age and ethnicity.
extrinsic factors such as UVR and certain chemical agents
intrinsic factors such as molecules secreted by neighboring keratinocytes, hormonal secretion, fibroblasts, inflammatory processes, pregnancy, or diabetes (Figure 7) [16].
Figure 7.
Association of keratinocytes and melanocytes. Synthesis of melanin and its transfer to keratinocytes taken from open access article: Signaling pathways in Melanogenesis.
Melanin is formed from the amino acid tyrosine through a series of chemical and enzymatic reactions described in the Raper-Mason pathway [32]. The end result of this pathway is the formation of two possible types of melanin: Eumelanin (dark brown/black color) and Pheomelanin (reddish/blond color).
In the structure of the melanocytes, we find the melanosomes, which are organelles where melanin is synthesized and stored before being distributed by keratinocytes.
From the L-tyrosine originated from the hydroxylation of L-phenylalanine, the melanin synthesis process begins, the enzyme tyrosinase hydroxylates L-tyrosine to 3.4 L dihydroxy-phenylalanine (L DOPA), which is then oxidized to dopaquinone by this same enzyme.
The enzyme tyrosinase is a copper-dependent enzyme, and it needs copper for its proper function (Figure 8) [16, 31, 32, 33].
Figure 8.
Pathway showing the synthesis of different forms of melanin from amino acid tyrosine by the enzyme tyrosinase. Open access
Vitamin C inhibits the synthesis of melanin by binding to the Copper (Cu) ions present in the melanogenesis pathway, thereby inhibiting the action of the tyrosinase enzyme which as we have commented is copper-dependent, the consequence is a reduction of melanin formation. To this effect of tyrosinase inhibition is added the suppression of oxidative polymerization of intermediates that occur in the pathway of melanin synthesis.
Unlike other active ingredients with depigmenting action, vitamin C is not cytotoxic against melanocytes [34, 35, 36].
Different split face studies support the efficacy of the use of 5% vitamin C as a topical depigmenting agent versus 4% hydroquinone, and although the results were lower compared to hydroquinone, the skin irritation produced by topical ascorbic acid was much less than that produced by topical ascorbic acid, by topical hydroquinone [37].
10.3 Anti-aging
One of the roles played by vitamin C in the body is to help maintain the collagen network. The mechanisms that allow this regulation and that justify its use as an antiaging treatment are listed below:
It prevents the autoinactivation of lysyl and prolil hydroxylase enzymes, key enzymes in the process of collagen synthesis, and its physiological reticulation at cellular and tissue level [38].
It directly activates the transcription of the factors involved in collagen synthesis and stabilizes messenger RNA (mRNA), which regulates the synthesis of type I and III collagens [19].
It increases the activity of the collagen expression gene by increasing the synthesis of the tissue inhibitor of MMP-1 and, consequently, decreases collagen degradation [18].
10.4 Regenerator of oxidized vitamin E
In our body, reactive oxygen species (ROS) are being generated continuously, to avoid their negative effects, we need them to be neutralized, and this work is carried out by two different families of scavengers:
Enzymatic scavengers such as glutathione peroxidase, superoxide dismutase, and catalases.
Non-enzymatic scavengers such as β-carotene, vitamin C, and vitamin E, both groups of scavengers are selenium dependent [39].
Vitamin E is a fat-soluble antioxidant composed of 4 tocopherols and 4 trienols, alpha-tocopherol being the most abundant form. Its function is to protect cell membranes from oxidative stress. The transport of vitamin E to the deeper layers of the stratum corneum is done through the secretion of sebaceous glands.
A single suberythematogenic sun exposure can deplete these skin vitamin E levels. Many human and animal trials support that topical use of vitamin E reduces lipid peroxidation, photoaging, immunosuppression, and photocarcinogenesis [19].
We know that both vitamin C and vitamin E have an antioxidant effect on the skin and reduce oxidative stress, interacting with each other, in such a way that vitamin C regenerates oxidized vitamin E, favoring the maintenance of the skin’s antioxidant reservoir [40].
The combination of 15% L-ascorbic acid and 1% tocopherol provides significant protection against postexposure erythema and sunburn, much greater when they act synergistically than separately [41].
11. Future developments
The cosmetic industry is still faced with the challenge of developing a more stable formulation and finding a method of transepidermal administration that increases the concentration of vitamin C in the skin, and, therefore, its effectiveness and results.
It has been shown that its oral or intravenous use at high doses, for example, 3 g/day, favors an increase in its concentration in the buccal mucosa, but its effectiveness on the skin has not been sufficiently clarified; by contrast, it has been observed a reduction in the presence of glutathione (tripeptide with antioxidant action) secondary to the use of doses of vitamin C that exceed the recommendations for daily intake [42].
We have studies that have shown that ultrasound, iontophoresis, fractional lasers of different types, and microdermabrasion can favor the skin penetration of vitamin C, but more research is needed and with larger samples to be able to evaluate the efficacy of using these routes versus topical [43].
Different types of studies are being conducted that allow us to expand the uses of vitamin C in treatments for hair loss, wound healing, scars, skin aging linked to smoking or other factors, and stretch marks [44].
12. Side effects and contraindications
Reviewing the literature, we can find some described adverse effects, especially with the oral intake of high amounts of vitamin C.
Some of them are nausea, vomiting, heartburn, colic, diarrhea, and oxalate kidney stones in predisposed patients, and with intakes above 3000 mg/day [45], although at this point, there is no unanimity among the different bibliographies [46].
Cases of topical vitamin C contact dermatitis have been reported in patients who tolerated it perfectly orally [47].
Oral vitamin C supplementation during pregnancy decreases the risk of placental abruption by 36%. Vitamin C is not teratogenic and its topical use is not contraindicated in pregnancy, and the associated use of sunblock is recommended on a daily basis, as the hormonal influence on melanogenesis was already discussed in a previous section [48]. In the case of pregnancy, it is vital to prevent the appearance of melasma, which can appear in up to 75% of women in the gestational state [49].
13. Conclusions
At this point in the chapter, the importance of vitamin C in human health and its great variety of biochemical functions is unquestionable. Reading of the previous sections leads us to the following conclusions.
It is a water-soluble vitamin that we cannot synthesize in our body, we need an external contribution through diet, in the form of supplements or topical application as cosmetic treatment or treatment of any pathology.
Ascorbic acid is found in different fruits (oranges, grapefruit, guava, macu macu, melon, strawberries...), red peppers, green peppers, broccoli, and tomatoes [50].
It is photosensitive but has no photosensitizing action.
Antioxidant action by MMP regulation.
Depigmenting action by inhibition of the tyrosinase enzyme.
Skin antiaging action.
Regenerative action of oxidized vitamin E.
Effective topically in improving wrinkles, hyperpigmentation, and scarring and as an antioxidant.
Reduces inflammation and UV-induced immunosuppression.
It inhibits the formation of melanin.
Photoprotective effect.
Its association with vitamin E enhances its action as a photoprotector.
Its cosmetic effectiveness is manifested in concentrations between 8% and 20%. Higher concentrations are not effective and produce skin irritation.
Cosmetics using this range of concentrations have shown their usefulness in treating the signs of skin aging.
Proven effectiveness in topical use.
It is necessary to find more stable chemical forms with greater skin penetration, and technology to increase its passage through the epidermis.
Conflict of interest
The author declares no conflict of interest.
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Available from: https://ods.od.nih.gov/factsheets/VitaminC-HealthProfessional/