Topical vitamin D3: A randomized controlled trial (RCT)

Bubshait, Dalal A.; Al-Dakheel, Dakheel A.; AlAnii, Fawaz M

doi:10.1016/j.clnesp.2018.05.009

Cited by 15 publications

(15 citation statements)

References 24 publications

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“…The protective effects of natural compounds show a significant impact on skin in various treatment regimen including pre- and post-treatment [94]. The post-treatment regimen has been used for vitamin D 3 treatment with some diseases including skin protection [95,96]. During the post-treatment, vitamin D 3 reduced the apoptosis and healing process in psoriasis [95].…”

Section: Discussionmentioning

confidence: 99%

“…During the post-treatment, vitamin D 3 reduced the apoptosis and healing process in psoriasis [95]. Additionally, the post-treatment with topical vitamin D 3 has been used in clinical trial as well [96]. Therefore, we found that it is important to test the effect of compounds in protection against UV-induced skin damage when used in both pre-treatment and post-treatment.…”

Section: Discussionmentioning

confidence: 99%

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Protective effects of novel derivatives of vitamin D3 and lumisterol against UVB-induced damage in human keratinocytes involve activation of Nrf2 and p53 defense mechanisms

et al. 2019

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We tested whether novel CYP11A1-derived vitamin D 3 - and lumisterol-hydroxyderivatives, including 1,25(OH) 2 D 3 , 20(OH)D 3 , 1,20(OH) 2 D 3 , 20,23(OH) 2 D 3 , 1,20,23(OH) 3 D 3 , lumisterol, 20(OH)L 3 , 22(OH)L 3 , 20,22(OH) 2 L 3 , and 24(OH)L 3 , can protect against UVB-induced damage in human epidermal keratinocytes. Cells were treated with above compounds for 24 h, then subjected to UVB irradiation at UVB doses of 25, 50, 75, or 200 mJ/cm 2 , and then examined for oxidant formation, proliferation, DNA damage, and the expression of genes at the mRNA and protein levels. Oxidant formation and proliferation were determined by the DCFA-DA and MTS assays, respectively. DNA damage was assessed using the comet assay. Expression of antioxidative genes was evaluated by real-time RT-PCR analysis. Nuclear expression of CPD, phospho-p53, and Nrf2 as well as its target proteins including HO-1, CAT, and MnSOD, were assayed by immunofluorescence and western blotting. Treatment of cells with the above compounds at concentrations of 1 or 100 nM showed a dose-dependent reduction in oxidant formation. At 100 nM they inhibited the proliferation of cultured keratinocytes. When keratinocytes were irradiated with 50–200 mJ/cm 2 of UVB they also protected against DNA damage, and/or induced DNA repair by enhancing the repair of 6-4PP and attenuating CPD levels and the tail moment of comets. Treatment with test compounds increased expression of Nrf2-target genes involved in the antioxidant response including GR , HO-1 , CAT , SOD1, and SOD2 , with increased protein expression for HO-1, CAT, and MnSOD. The treatment also stimulated the phosphorylation of p53 at Ser-15, increased its concentration in the nucleus and enhanced Nrf2 translocation into the nucleus. In conclusion, pretreatment of keratinocytes with 1,25(OH) 2 D 3 or CYP11A1-derived vitamin D 3 - or lumisterol hydroxy-derivatives, protected them against UVB-induced damage via activation of the Nrf2-dependent antioxidant response and p53-phosphorylation, as well as by the induction of the DNA repair system. Thus, the new vitamin D 3 and lumisterol hydroxy-derivatives represent promising anti-photodamaging agents.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Protective effects of novel derivatives of vitamin D3 and lumisterol against UVB-induced damage in human keratinocytes involve activation of Nrf2 and p53 defense mechanisms

et al. 2019

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show abstract

“…The protective effects of natural compounds show a significant impact on skin in various treatment regimen including pre-and posttreatment [94]. The post-treatment regimen has been used for vitamin D 3 treatment with some diseases including skin protection [95,96].…”

Section: Discussionmentioning

confidence: 99%

Protective effects of novel derivatives of vitamin D3 and lumisterol against UVB-induced damage in human keratinocytes involve activation of Nrf2 and P53 defense mechanisms

Chaiprasongsuk

Kim

Holick

et al. 2018

Free Radical Biology and Medicine

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We tested whether novel CYP11A1-derived vitamin D 3-and lumisterol-hydroxyderivatives, including 1,25(OH) 2 D 3 , 20(OH)D 3 , 1,20(OH) 2 D 3 , 20,23(OH) 2 D 3 , 1,20,23(OH) 3 D 3 , lumisterol, 20(OH)L 3 , 22(OH)L 3 , 20,22(OH) 2 L 3 , and 24(OH)L 3 , can protect against UVB-induced damage in human epidermal keratinocytes. Cells were treated with above compounds for 24 h, then subjected to UVB irradiation at UVB doses of 25, 50, 75, or 200 mJ/cm 2 , and then examined for oxidant formation, proliferation, DNA damage, and the expression of genes at the mRNA and protein levels. Oxidant formation and proliferation were determined by the DCFA-DA and MTS assays, respectively. DNA damage was assessed using the comet assay. Expression of antioxidative genes was evaluated by real-time RT-PCR analysis. Nuclear expression of CPD, phospho-p53, and Nrf2 as well as its target proteins including HO-1, CAT, and MnSOD, were assayed by immunofluorescence and western blotting. Treatment of cells with the above compounds at concentrations of 1 or 100 nM showed a dose-dependent reduction in oxidant formation. At 100 nM they inhibited the proliferation of cultured keratinocytes. When keratinocytes were irradiated with 50-200 mJ/cm 2 of UVB they also protected against DNA damage, and/or induced DNA repair by enhancing the repair of 6-4PP and attenuating CPD levels and the tail moment of comets. Treatment with test compounds increased expression of Nrf2-target genes involved in the antioxidant response including GR, HO-1, CAT, SOD1, and SOD2, with increased protein expression for HO-1, CAT, and MnSOD. The treatment also stimulated the phosphorylation of p53 at Ser-15, increased its concentration in the nucleus and enhanced Nrf2 translocation into the nucleus. In conclusion, pretreatment of keratinocytes with 1,25(OH) 2 D 3 or CYP11A1-derived vitamin D 3-or lumisterol hydroxy-derivatives, protected them against UVB-induced damage via activation of the Nrf2-dependent antioxidant response and p53-phosphorylation, as well as by the induction of the DNA repair system. Thus, the new vitamin D 3 and lumisterol hydroxy-derivatives represent promising anti-photodamaging agents.

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“…Apart from oral intake, vitamin D can also be administered intramuscularly with a similar, yet delayed, increase compared to oral intakes (134, 135, 136). Transdermal applications of vitamin D do also raise serum 25(OH)D, but more data on this topic are needed (137, 138). Apart from vitamin D, there are also 25(OH)D preparations available for treatment that are about 3.2–5-fold as effective as vitamin D in raising serum 25(OH)D concentrations (139, 140).…”

Section: Practical Vitamin D Testing and Supplementationmentioning

confidence: 99%

Vitamin D testing and treatment: a narrative review of current evidence

Pilz

Zittermann

Trummer

et al. 2019

Endocrine Connections

204

154

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Vitamin D testing and treatment is a subject of controversial scientific discussions, and it is challenging to navigate through the expanding vitamin D literature with heterogeneous and partially opposed opinions and recommendations. In this narrative review, we aim to provide an update on vitamin D guidelines and the current evidence on the role of vitamin D for human health with its subsequent implications for patient care and public health issues. Vitamin D is critical for bone and mineral metabolism, and it is established that vitamin D deficiency can cause rickets and osteomalacia. While many guidelines recommend target serum 25-hydroxyvitamin D (25[OH]D) concentrations of ≥50 nmol/L (20 ng/mL), the minimum consensus in the scientific community is that serum 25(OH)D concentrations below 25–30 nmol/L (10–12 ng/mL) must be prevented and treated. Using this latter threshold of serum 25(OH)D concentrations, it has been documented that there is a high worldwide prevalence of vitamin D deficiency that may require public health actions such as vitamin D food fortification. On the other hand, there is also reason for concern that an exploding rate of vitamin D testing and supplementation increases costs and might potentially be harmful. In the scientific debate on vitamin D, we should consider that nutrient trials differ from drug trials and that apart from the opposed positions regarding indications for vitamin D treatment we still have to better characterize the precise role of vitamin D for human health.

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Topical vitamin D3: A randomized controlled trial (RCT)

Abstract: The results of this study indicate that transdermal route of vitamin D is potentially, safe and can give desired results to raise the vitamin D levels. This route is an alternate route for supplementation of vitamin D which should be utilized.

Cited by 15 publications

References 24 publications

Protective effects of novel derivatives of vitamin D3 and lumisterol against UVB-induced damage in human keratinocytes involve activation of Nrf2 and p53 defense mechanisms

Protective effects of novel derivatives of vitamin D3 and lumisterol against UVB-induced damage in human keratinocytes involve activation of Nrf2 and p53 defense mechanisms

Protective effects of novel derivatives of vitamin D3 and lumisterol against UVB-induced damage in human keratinocytes involve activation of Nrf2 and P53 defense mechanisms

Vitamin D testing and treatment: a narrative review of current evidence

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