Abstract
The significance of Coenzyme Q10 (CoQ10) as an anti-oxidant barrier of the skin, as well as a key component in anti-aging strategies for skin care products, has been firmly established. Biosynthesis of CoQ10 in the mitochondria is well known, but there is only limited information on the non-mitochondrial synthesis of CoQ10 in the skin. Recent findings in zebrafish identified that a tumor suppressor, Ubiad1, is also a key enzyme in the non-mitochondrial synthesis of CoQ10. The purpose of this study was to investigate expression of Ubiad1 in human skin, and its implication in the skin’s cutaneous response to oxidative stress. We observed Ubiad1 localization in the epidermis, particularly a subcellular localization in the Golgi apparatus. Ubiad1 modulation by a pentapeptide was associated with an observed reduction in ROS/RNS stresses (−44%/−19% respectively), lipid peroxidation (−25%) and preservation of membrane fluidity under stress conditions. Electron microscopy of keratinocytes revealed a significant degree of stimulation of the Golgi complex, as well as significantly improved mitochondrial morphology. Given the importance of CoQ10 in mitigating the visible signs of skin aging, our findings identify Ubiad1 as an essential component of the defensive barriers of the epidermis.
Highlights
Human skin is acutely and chronically exposed to natural and anthropogenic stressors such as ultraviolet radiation, pollutants and chemical organic toxicants, all of which induce varying levels of oxidative stress
The present study demonstrates that Ubiad1 is an enzyme expressed in spinous and basal layers of the epidermis; and that its expression reduces during the epidermal differentiation process
Because the effectiveness of endogenous antioxidant systems is diminished during aging, Ubiad1 modulation represents a key aspect for future considerations in the field of skin aging
Summary
Human skin is acutely and chronically exposed to natural and anthropogenic stressors such as ultraviolet radiation, pollutants and chemical organic toxicants, all of which induce varying levels of oxidative stress. Oxidative stress is associated with the generation of excessive amounts of superoxide anion, hydrogen peroxide and hydroxyl radicals [1], which causes the skin to exhibit signs of premature aging by imparting a variety of physical and physiological damage. The first line of defense, possess antioxidant molecules such as vitamin E, coenzyme Q10 (CoQ10) and ascorbate [2]. Chronological aging causes a decline in the efficiency of endogenous antioxidative mechanisms and repair processes in general [3], as documented by extensive academic and industry research.
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