Cutaneous ageing is a complex biological process influenced by a combination of endogenous or intrinsic (e.g. genetics, cellular metabolism, hormone and metabolic processes) and exogenous or extrinsic (e.g. chronic light exposure, pollution, ionising radiation, chemicals, toxins) factors, primarily due to UV/photo damage.1 Many studies have helped us better understand the difference between chronological ageing and photoageing.
Chronological skin ageing is characterised by laxity and fine wrinkling, as well as seborrheic keratoses. However, it is not associated with increased pigmentation or deep wrinkles that characterise photoageing. The term ‘photoageing’ was first coined in 1986 and it describes the effects under chronic ultraviolet radiation.2 In fact, the concept of photoageing includes chronological ageing and the outcomes from exposure of skin to UV radiation. Photoageing is characterised by coarse and deep wrinkling, mottled pigmentation, sallowness, dryness, textural roughness, telangiectasias and the laxity of the skin. The last feature, laxity of the skin, is also one of the features that are attributed to chronological skin ageing.
The damage from ultraviolet radiation on skin is due, in part, to the generation of reactive oxygen species (ROS) and causes immediate sunburn reaction to chronic effects such as photoageing. When skin is exposed to the sun, UV penetrates the skin’s epidermis, leading to the generation of free radicals like ROS. Then, excessive ROS stimulates the inflammatory process of skin, such as inflammatory cytokines (interleukin-1a, interleukin-6 and interleukin-8), COX-2, iNOS and NO. The increase of inflammatory cytokines, in turn, releases the matrix metalloproteinase (MMP), which is fibroblast collagenase mediating collagen degradation, wrinkle formation, and eventually premature ageing.3 In photoageing processes, UVB is the main culprit, since it also induces damage in epidermal DNA and increase sunburn cell formation within the epidermal layer. Thus protecting DNA is another key to protecting and preventing skin from ageing.
Et-VCTM, 3-O-ethyl ascorbic acid, is a multi-functional vitamin C derivative with better stability, and it is metabolised the same way as ascorbic acid in our body. From our previous studies, Et-VC can provide superb whitening effects via free radical activity inhibition, tyrosinase activity inhibition, and melanin inhibition. To further investigate the function of Et-VC (now referred to as ‘the new vitamin C derivative’) on anti-ageing, there are several new findings demonstrating the ability of the new vitamin C derivative to prevent photoageing (anti-inflammation), stimulate collagen synthesis, protect DNA, reduce wrinkles, minimise the cheek sebaceous pores, enhance skin suppleness, as well as in photoprotection.
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