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Since the Vitamin C in the form of ascorbic acid is very unstable against any light and air, if used in cosmetic products, after production and over time, the percentage of this substance in the product decreases. In this Recommended product (Universal ReyLaku Vitamin C 20% serum ) , we have tried to keep the percentage of vitamin C constant during the period of customer use and exactly according to our claims on the product packaging. We have used the following simple method:
However, all the contents of the case and the bottle are completely stable for 3 years before mixing. This technology has been used for many years in products around the world, the most famous of which is the 15% vitamin C lotion of DUOLYS ACM France, in which the ascorbic acid case is embedded in the end of the bottle.
Vitamin C is one of the naturally occurring antioxidants in nature.Most plants and animals are able to synthesise Vitamin C in vivo from glucose. Humans and certain other vertebrates lack the enzyme L glucono gamma lactone oxidase required for in vivo synthesis of Vitamin C hence, they must acquire it from natural sources such as citrus fruits, green leafy vegetables, strawberries, papaya and broccoli. Traditionally, Vitamin C rich foods like lemons were carried by sailors on long journeys to avoid Scurvy, a disease of bleeding gums. 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.
L ascorbic acid (LAA) is the chemically active form of Vitamin C. In nature, Vitamin C is found in equal parts as LAA and D ascorbic acid. These are essentially isomeric molecules and are mutually interchangeable. However, only LAA is biologically active and thus useful in medical practice. The absorption of Vitamin C in the gut is limited by an active transport mechanism and hence a finite amount of the drug is absorbed despite high oral dosage. Furthermore, bioavailability of Vitamin C in the skin is inadequate when it is administered orally. The use of topical ascorbic acid is therefore favored in the practice of dermatology.
Vitamin C has a 5 hydrocarbon ring similar to that of glucose. With an attached hydrogen ion, LAA becomes a weak sugar acid, similar to other Alfa Hydroxy acids used in dermatology. With a metal ion, it forms a mineral ascorbate. There is a marked interest in synthesis of physiologically active and chemically stable ascorbate molecules as LAA is unstable in nature, especially when exposed to light.
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. 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 neutralize the free radicals. The oxidised forms of Vitamin C are relatively non-reactive. Furthermore, they can be converted back to Vitamin C 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.
As mentioned above, the exposure of skin to UV light generates ROS. These radicals 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 metaloprotienase (MMP) production, leading to collagen breakdown. Oxidative stress induces nuclear transcription factor kappa B (NFkB). This produces a number of mediators that contribute to inflammation and skin ageing. ROS also increase the elastin mRNA level in dermal fibroblasts. This may explain the elastotic changes observed in photoaged skin.
Antioxidants are necessary for neutralizing 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). Repeated small doses of UVA penetrate 30-40-times deeper into the dermis as against UVB, which mostly affects the epidermis. UVA mutates and destroys collagen, elastin, proteoglycans and other dermal cellular structures. Thus, UVA causes skin ageing and possibly melanoma formation. 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, sunscreens block only 55% of the free radicals produced by UV exposure. Photoageing can be prevented by prevention of UV-induced erythema, sunburn cell formation and inducing collagen repair. To optimize UV protection, it is important to use sunscreens combined with a topical antioxidant. Vitamin C does not absorb UV light but exerts an UV-protective effect by neutralizing free radicals, while this effect is not seen with sunscreens. Under laboratory conditions, it has been shown that application of 10% topical Vitamin C showed statistical reduction of UVB-induced erythema by 52% and sunburn cell formation by 40-60%.
Although Vitamin C alone can provide photoprotection, it works best in conjunction with Vitamin E, which potentiates the action of Vitamin C four-fold. Hydrophilic Vitamin C helps regenerate Vitamin E, a liphophilic antioxidant. Thus, Vitamin C and Vitamin E together protect the hydrophilic and lipophilic compartments of the cell, respectively. Vitamin C and Vitamin E synergistically limit chronic UV damage by significantly reducing both cell apoptosis and thymine dimer formation.
Vitamin C is essential for collagen biosynthesis. It has been proposed that Vitamin C influences quantitative collagen synthesis in addition to stimulating qualitative changes in the collagen molecule. Vitamin C serves as a co-factor for the enzymes prolysyl and lysyl hydroxylase, the enzymes that are responsible for stabilizing and cross-linking the collagen molecules. Another mechanism by which Vitamin C influences the collagen synthesis is by stimulation of lipid peroxidation, and the product of this process, malondialdehyde, in turn stimulates collagen gene expression.
Vitamin C also directly activates the transcription of collagen synthesis and stabilizes procollagen mRNA, thereby regulating collagen synthesis. Signs and symptoms of Scurvy, a deficiency disease of Vitamin C, are due to impaired collagen synthesis. Clinical studies have shown that the topical use of Vitamin C increases collagen production in young as well as aged human skin.