Abstract
This animal study aimed to elucidate the relationship of low-dose, narrow-band UVB at 308 nm with vitamin D synthesis. C57BL/6 female mice, at 3 weeks-of-age, were randomly divided into the following six groups (n = 6 at each time point of vitamin D measurement), which were: (1) normal diet without UVB irradiation; (2) VDd diet without UVB irradiation; and (3)–(6) VDd diet with 308 nm-UVB irradiation of 12.5, 25, 50, and 100 μω/cm2, respectively. All of the groups needing UVB irradiation received an exposure of 10 min per day, five days per week, and a duration of 3–5 weeks. The mice recovering from severe VDd (plasma total 25-hydroxyvitamin D level increasing from approximately 3 to over 30 ng/mL) only occurred in groups with a UVB irradiation dosage of either 50 or 100 μω/cm2. The optimal, estimated dosage for mice to recover from severe VDd was 355 mJ/cm2 within 3 weeks. Low-dose, narrow-band UVB irradiation at 308 nm is effective in improving VDd in mice. The results obtained, in addition to the especially small side effects of the above UVB irradiation formula, could be further translated to treating VDd-related disorders.
Highlights
This animal study aimed to elucidate the relationship of low-dose, narrow-band ultraviolet B (UVB) at 308 nm with vitamin D synthesis
After 2 week of UVB irradiation, the vitamin D deficiency (VDd) with 100 μω/cm[2] group had its serum 25(OH)D levels dramatically improved to normal, and maintained this level at 3 week with no significant difference when compared with the normal diet group
In the VDd with 12.5 μω/cm[2] UVB irradiation group, which was the lowest exposure, its 25(OH)D levels were never higher than 15 ng/mL, and maintained a level of approximately 10 ng/ml for the remainder of the measured points after 2 week
Summary
This animal study aimed to elucidate the relationship of low-dose, narrow-band UVB at 308 nm with vitamin D synthesis. Vitamin D is produced in the epidermis by photochemical transformation, where 7-dehydrocholesterol is subsequently hydroxylated to prduce biologically active 1α,25-dihydroxyvitamin D (1,25(OH)2D3)[5,6]. In this canonical pathyways, vitamin D is transported to the liver where it is hydroxylated at C25 by CYP27A1 or CYP2R1 to form 25(OH)D3. CYP11A1 acts on 7-dehydrocholesterol (7DHC) producing 22(OH)7DHC, 20,22(OH)27DHC and 7-dehydropregnenolone which can be converted to the vitamin D and L3 configurations following exposure to U VB13 These CYP11A1derived compounds are detected in human epidermis and serum, and pig adrenal gland, and are biologically active displaying anti-proliferative, anti-inflammatory, anti-cancer and pro-differentiation p roperties[14]
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