Oral phytochemicals as photoprotectants in UVR exposed hairless mice: A study of hesperidin methyl chalcone, phloroglucinol, and syringic acid

Pihl, Celina; Bendtsen, Katja Maria; Jensen, Henrik Elvang; Andersen, F. Alan; Bjerring, Peter; Hædersdal, Merete; Lerche, Catharina M.

doi:10.1016/j.jphotobiol.2023.112760

Cited by 3 publications

(7 citation statements)

References 47 publications

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“…Hairless C3.Cg-Hr hr /TifBomTac mice (n = 100; age 17-30 weeks) were purchased from Taconic (Ry, Denmark). The mice were acclimatised for at least 4 weeks in facilities as reported in previous studies [15,24]. Mice were randomised into four groups, receiving either a standard dose of NAM-mono (600 mg/kg) [15], NAM (400 mg/kg) + Met (200 mg/kg), NAM (400 mg/kg) + PG (75 mg/kg), or no supplementation as the UV control.…”

Section: Study Overview and Treatmentsmentioning

confidence: 99%

“…The mice were acclimatised for at least 4 weeks in facilities as reported in previous studies [15,24]. Mice were randomised into four groups, receiving either a standard dose of NAM-mono (600 mg/kg) [15], NAM (400 mg/kg) + Met (200 mg/kg), NAM (400 mg/kg) + PG (75 mg/kg), or no supplementation as the UV control. All treatments were delivered daily through the drinking water.…”

Section: Study Overview and Treatmentsmentioning

confidence: 99%

“…Mice were irradiated with UVR three times each week to induce tumour development. A dose of 3.5 standard erythema doses was administered as previously reported [15,24], emitting 5.9% within the UVB range. Mice were checked each week for the development of tumours and any new appearances at 1 mm in diameter or above were recorded.…”

Section: Irradiation Protocol and Tumour Developmentmentioning

confidence: 99%

“…The 3 tumours that first reached 4 mm were used to determine the median time till tumour onset. Tumours that did not reach 4 mm were not included in further analysis of tumour number or tumour area determined as follows [15]:…”

Section: Irradiation Protocol and Tumour Developmentmentioning

confidence: 99%

“…Oral photoprotection has gained interest in an effort to overcome poor adherence to classical skin cancer prevention measures [14]. We have recently shown that oral supplementation with both nicotinamide and the brown algaederived compound phloroglucinol reduces UVR-induced carcinogenesis in hairless mice [15]. Nicotinamide functions as a photoprotectant by enhancing DNA repair [16].…”

Section: Introductionmentioning

confidence: 99%

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Efficacy of Combinational Treatment versus Nicotinamide Monotherapy in the Prevention of Ultraviolet Radiation-Induced Skin Cancer

Pihl,

Andersen,

Bjerring

et al. 2024

Dermatology

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Introduction: Ultraviolet radiation (UVR) is the primary risk factor for keratinocyte carcinomas. Oral supplementation with nicotinamide (NAM) is reported to reduce the formation of new keratinocyte carcinomas. NAM’s photoprotection is mediated by enhanced DNA repair. We wanted to explore whether NAM in combination with antiproliferative (metformin [Met]) or antioxidant (phloroglucinol [PG]) compounds could potentially enhance its photoprotective effects. Methods: Hairless mice (C3.Cg-Hrhr/TifBomTac) were treated orally with either a standard dose of NAM monotherapy (NAM-mono; 600 mg/kg) or NAM (400 mg/kg) combined with Met (200 mg/kg) (NAM-Met) or PG (75 mg/kg) (NAM-PG). Mice were irradiated with 3.5 standard erythema doses of UVR three times per week to induce tumour development. Photoprotective effects were based on (i) tumour onset of the first three tumours, (ii) skin photodamage, and (iii) DNA damage (cyclobutane pyrimidine dimers [CPDs] and pyrimidine-pyrimidone (6–4) photoproducts [6-4PPs]). Results: All mice treated with NAM demonstrated a delay in tumour onset and reduced tumour burden compared to the UV control group (NAM, NAM-Met, NAM-PG vs. UV control: p ≤ 0.015). NAM-mono and NAM-PG increased time until all three tumours with no difference between them, indicating a similar degree of photoprotection. NAM-mono had no effect on DNA damage compared to the UV control group (p > 0.05), whereas NAM-PG reduced 6-4PP lesions (p < 0.01) but not CPDs (p > 0.05) compared to NAM-mono. NAM-Met delayed the onset of the third tumour compared to the UV control but demonstrated a quicker onset compared to NAM-mono, suggesting inferior photoprotection compared to nicotinamide monotherapy. Conclusion: NAM-PG was as effective in delaying UVR-induced tumour onset as NAM-mono. The reduction in 6-4PP lesions may indicate that the mechanism of NAM-PG is better suited for photoprotection than NAM-mono. NAM-mono was superior to NAM-Met, indicating a dose dependency of NAM’s photoprotection. These results highlight the potential for combining photoprotective compounds to enhance photoprotection.

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Section: Study Overview and Treatmentsmentioning

confidence: 99%

Section: Study Overview and Treatmentsmentioning

confidence: 99%

Section: Irradiation Protocol and Tumour Developmentmentioning

confidence: 99%

Section: Irradiation Protocol and Tumour Developmentmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Efficacy of Combinational Treatment versus Nicotinamide Monotherapy in the Prevention of Ultraviolet Radiation-Induced Skin Cancer

Pihl,

Andersen,

Bjerring

et al. 2024

Dermatology

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Oral intake of bucillamine, carvedilol, metformin, or phenformin does not protect against UVR-induced squamous cell carcinomas in hairless mice

Pihl,

Bjerring,

Andersen

et al. 2024

Photochem Photobiol Sci

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Squamous cell carcinoma represents the second most common type of keratinocyte carcinoma with ultraviolet radiation (UVR) making up the primary risk factor. Oral photoprotection aims to reduce incidence rates through oral intake of photoprotective compounds. Recently, drug repurposing has gained traction as an interesting source of chemoprevention. Because of their reported photoprotective properties, we investigated the potential of bucillamine, carvedilol, metformin, and phenformin as photoprotective compounds following oral intake in UVR-exposed hairless mice. Tumour development was observed in all groups in response to UVR, with only the positive control (Nicotinamide) demonstrating a reduction in tumour incidence (23.8%). No change in tumour development was observed in the four repurposed drug groups compared to the UV control group, whereas nicotinamide significantly reduced carcinogenesis (P = 0.00012). Metformin treatment significantly reduced UVR-induced erythema (P = 0.012), bucillamine and phenformin increased dorsal pigmentation (P = 0.0013, and P = 0.0005), but no other photoprotective effect was observed across the repurposed groups. This study demonstrates that oral supplementation with bucillamine, carvedilol, metformin, or phenformin does not affect UVR-induced carcinogenesis in hairless mice. Graphical Abstract

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Oral administration of quercetin and fisetin potentiates photocarcinogenesis in UVR-exposed hairless mice

Pihl,

Granborg,

Pinto

et al. 2024

Phytomedicine Plus

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Oral phytochemicals as photoprotectants in UVR exposed hairless mice: A study of hesperidin methyl chalcone, phloroglucinol, and syringic acid

Cited by 3 publications

References 47 publications

Efficacy of Combinational Treatment versus Nicotinamide Monotherapy in the Prevention of Ultraviolet Radiation-Induced Skin Cancer

Efficacy of Combinational Treatment versus Nicotinamide Monotherapy in the Prevention of Ultraviolet Radiation-Induced Skin Cancer

Oral intake of bucillamine, carvedilol, metformin, or phenformin does not protect against UVR-induced squamous cell carcinomas in hairless mice

Oral administration of quercetin and fisetin potentiates photocarcinogenesis in UVR-exposed hairless mice

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