SKIN CARE
Vitamin C in skin care applications: An overview
Dr Cuross Bakhtiar - Harley Street Cosmetic Dr Iftikhar Khan - Liverpool John Moores University
Vitamin C (Figure 1) is a naturally occurring antioxidant.1,2
ABSTRACT Most plants and animals are able
to acquire it in vivo from glucose (Figure 2 & 3). However, humans and certain vertebrates lack the L-glucono-gamma lactone oxidase enzyme required to do this and must instead acquire synthesise vitamin C from natural sources such as citrus fruits, green leafy vegetables, strawberries, papaya and broccoli.3,4 Traditionally, vitamin C-rich foods
like lemons were carried by sailors on long journeys to avoid scurvy. In 1937, Dr Albert Szent Goyrgi was awarded the Nobel Prize for his work in isolating the vitamin C molecule from red peppers and identifying its role in scurvy.4 In nature, vitamin C is found in equal parts as L- and D-ascorbic acid (LAA, DAA). These are essentially isomeric molecules and are mutually interchangeable, but only LAA is biologically active and thus useful in biochemistry.2,4 The absorption of vitamin C in the gut is
limited by an active transport mechanism and hence a finite amount of it is absorbed, even if a high oral dosage is taken.3
Furthermore,
its bioavailability in the skin is inadequate when administered orally.1,2
The use of topical
ascorbic acid is therefore favoured in the practice of medicine.5 Vitamin C has a 5-hydrocarbon ring similar
to that of glucose (Figure 1). With an attached hydrogen ion, LAA becomes a weak sugar acid, similar to other α-hydroxy acids used in dermatology. With a metal ion, it forms a mineral ascorbate. There is a marked interest in the synthesis of physiologically active and chemically stable ascorbate molecules, as LAA is unstable in nature, especially when exposed to light.
Mechanism of action in dermatology Vitamin C, the most plentiful antioxidant in human skin, forms a part of the complex group of enzymatic and non-enzymatic antioxidants that co-exist to protect the skin from reactive oxygen species (ROS). As vitamin C is water-soluble, it functions in the aqueous compartments of the cell.4 When the skin is exposed to UV light,
ROS, such as the superoxide ion, peroxide and singlet oxygen, are generated. Vitamin C protects the skin from oxidative stress by sequentially donating electrons to neutralise
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Citrus fruit has long played a part in preventing scurvy by delivering more vitamin C to the body
the free radicals. The oxidised forms of vitamin C are relatively non-reactive.4
Furthermore,
they can be converted back by the enzyme dehydro-ascorbic acid reductase in the presence of glutathione. Exposure to UV light reduces the availability
of vitamin C in the skin. The exposure of skin to UV light also generates ROS, which have a potential to start chain or cascade reactions that damage the cells. The harmful effects of ROS occur as direct chemical alterations of the cellular DNA, the cell membrane and the cellular proteins, including collagen. Oxidative stress also triggers certain cellular
events mediated by transcription factors such as ROS upgrade transcription factor activator protien-1 (AP-1) that increases matrix metalloprotienase (MMP) production, leading to collagen breakdown. It induces nuclear transcription factor kB (NFkB). This produces a number of mediators that contribute to
OH H HO O O
Vitamin C is a potent antioxidant molecule that can be used topically to reduce the changes associated with photoageing. It can also be used for the treatment of hyperpigmentation. Because it is unstable and difficult to deliver into the dermis in the optimum dosage, research is being directed to finding stable compounds and newer methods of delivery (lipid-based micro and nano carrier systems) of vitamin C into the dermis.
inflammation and skin ageing.3 ROS also
increase the elastin mRNA level in dermal fibroblasts. This may explain the elastotic changes observed in photo-aged skin.2 Antioxidants are necessary for neutralising the
ROS formed due to UV exposure. It is important to note that vitamin C is equally effective against both UVB (290-320 nm) and UVA (320-400 nm).2-5 Repeated small doses of UVA penetrate 30-40 times deeper into the dermis than UVB, which mostly affects the epidermis. UVA mutates and destroys collagen, elastin, proteoglycans and other dermal cellular structures.2
Thus, it
causes skin ageing and possibly melanoma formation. Meanwhile, UVB causes sunburn, ROS, epidermal mutations and skin cancer. Sunscreens, when properly applied,
prevent UV-induced erythema and thymine dimer mutations that contribute to cutaneous carcinogenesis. However, they block only 55% of the free radicals produced by UV exposure. Photo-ageing can be prevented by preventing UV-induced erythema, sunburn cell formation and inducing collagen repair.2 To optimise UV protection, it is important
to use sunscreens combined with a topical antioxidant. Vitamin C does not absorb UV light but exerts a protective effect by neutralising free radicals, which is not seen with sunscreens. Under laboratory conditions, applying 10% topical vitamin C showed statistical reduction of UVB-induced erythema by 52% and sunburn cell formation by 40-60%.3 Vitamin C alone can provide photoprotection,
HO Figure 1: L-ascorbic acid OH
but it works best in conjunction with vitamin E, which boosts its action four-fold. Hydrophilic vitamin C in turn help to regenerate vitamin E, which is a lipophilic antioxidant.1,3,5,6 they protect the hydrophilic and lipophilic
Together, November 2021 PERSONAL CARE
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