Skin aging is the result of several factors such as intense physical and psychological stress, alcohol intake, poor nutrition, overeating, environmental pollution, and UV exposure. The speed of skin aging is determined by intrinsic and extrinsic factors.
- Intrinsic skin aging is determined primarily by genetic factors, hormonal status and metabolic reactions, such as oxidative stress. Skin is at risk for similar degenerative effects seen in other organs, yet due to its visibility, the skin outwardly discloses many aspects of our inner health.
- Extrinsic Factors - UV Radiation / "Photoaging" and environmental toxins.
One of the most important extrinsic factors accelerating skin aging is solar ultraviolet radiation (UVR). Excessive sun exposure is a primary causal factor in various skin diseases including premature aging, inflammatory conditions, melanoma and non-melanoma skin cancers (Chang 2010; Schmitt 2011).
Excess exposure of skin to UV causes a series of deleterious biochemical reactions in the skin - photoaging. Chronic sun exposure damages the dermal connective tissue and alters normal skin metabolism, depresses immunity, and stimulates oxidative stress and inflammation, etc. UV radiation increases the production of matrix metalloproteinases (MMPS), enzymes that degrade collagen (Taihao 2009), which causes loss of skin elasticity and firmness.
Environmental toxins include tobacco use and pollution. Studies have confirmed that smoking tobacco damages the skin via multiple mechanisms as well (Serri 2010). Epidemiological studies have correlated pollution levels with poor health status. Specifically, recent studies relate particle pollution to advanced skin aging. Most notably, skin hyperpigmentation and sluggish skin cell renewal has been observed in both human and animal studies (Pedata 2011; Vierkötter 2010).
The major targets of UV irradiation in the skin are the surface epidermal layers; eumelanin is the cellular factor mediating photoprotective effect on the epidermal cells. Cellular production of eumelanin is controlled by melanocortin receptor 1c (MC1R). a-MSH, ACTH, and a-MSH analogs enhance eumelanogenesis, thus induce sunless tanning helping reduce risk of melanoma and non-melanoma skin cancer. On the other hand, ASIP (targeting MR1C), oligopeptides with tyrosinase inhibitory activity, Lumixyl, octapeptides P16-18, kojic acid, and hormones inhibiting MITF pathway, IL-1, IL-6, and TGF-b, can reduce eumelanin production and pigmentation thus can be used for skin whitening.
Disclaimer
Information on this website is summarized from published literatures for education purpose only. All molecular structures listed are for example purposes but not meant to be used as ingredients in cosmetic products.
For regulatory policy of each molecule and its use for cosmetic product, please refer to the released information of FDA or your local government. All information is provided for informational and marketing purposes only.
