Astaxanthin Promotes Healthy Skin
Astaxanthin is one of nature's most powerful antioxidants with numerous health and beauty benefits.
* Astaxanthin is more effective than other antioxidants in trapping energy from singlet oxygen.
Astaxanthin, a xanthophyll carotenoid, is a secondary metabolite naturally synthesized by a number of bacteria, microalgae, and yeasts. To date, the microalga Haematococcus pluvialis has been the most promising source for its industrial biological production. Due to its collective diverse functions in skin biology, there is mounting evidence that astaxanthin possesses various health benefits and important nutraceutical applications in the field of dermatology. A range of potential mechanisms by which astaxanthin may exert its benefits on skin homeostasis have been proposed, including photoprotective, antioxidant, and anti-inflammatory effects.
Skin-Protective Mechanisms of Astaxanthin
The molecular and morphological changes in aging skin not only impair its protective role, but also lead to the appearance of skin symptoms, including excessive dryness and itching, increased predisposition to the formation or deepening of wrinkles, dyspigmentation, injury fragility and healing difficulties, impaired perception and responsiveness to mechanical stimuli, skin irritation, etc. Astaxanthin mainly promote healthy skin in the following ways [1].
Oxidative stress is a crucial factor affecting human skin aging and dermal damage. Intrinsic (time) aging through oxidative metabolism and extrinsic (light) aging through exposure of solar ultraviolet (UV) light may generate reactive oxygen species (ROS) which is a key mechanism leading to skin aging.
The photoprotective effects of carotenoids have demonstrated that astaxanthin is a superior antioxidant, having great antioxidant capacity in human dermal fibroblasts. Particularly, astaxanthin inhibits ROS formation and modulates the expression of oxidative stress-responsive enzymes such as heme oxygenase-1 (HO-1).
- Anti-inflammatory properties
Continued oxidative stress leads to chronic inflammation, which in turn, mediates most chronic diseases including neurodegeneration, cancer, and skin damage.
Astaxanthin has been proved to have the ability to promote healthy skin by decreasing UV-induced reactive nitrogen species production, inflammatory cytokine expression, and apoptosis in keratinocytes. Particularly, studies showed the ability of astaxanthin to inhibit the production of inflammatory mediators by blocking nuclear factor-κB (NF-κB) activation in human keratinocytes, indicating that astaxanthin may offer an attractive new strategy for treating skin inflammatory diseases.
A large amount of evidence suggests that suppression of immune system contributes to the development of solar UV-induced cutaneous malignancies.
Astaxanthin significantly affects immune function in several in vitro and in vivo assays. For example, in vitro studies on human lymphocytes have shown that astaxanthin enhances immunoglobulin production in response to T-cell-dependent stimulation. In addition to the cell-mediated immune response, astaxanthin also stimulated humoral immunity.
Skin exposure to ultraviolet radiation can cause DNA damage. The biologically harmful effects associated with UV radiation exposure are largely the result of errors in DNA repair, which can lead to oncogenic mutations.
Astaxanthin has been reported to improve the DNA repair capacity of cells exposed to UV radiation. Particularly, astaxanthin is capable of minimizing DNA damage and influencing the kinetics of DNA repair.
Astaxanthin is a promising compound in the field of dermatology due to its involvement in a variety of biological activities. Astaxanthin inhibits collagenase, MMP (matrix metalloproteinase) activity, inflammatory mediators, and ROS induction, producing potent anti-wrinkle and antioxidant effects. In addition, astaxanthin prevents UV-induced immunosuppression.
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Reference
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Davinelli, S., Nielsen, M., & Scapagnini, G. Astaxanthin in Skin Health, Repair, and Disease: A Comprehensive Review. Nutrients, 2018, 10(4), 522.
