Potentiating effect of dietary vitamin A on photocarcinogenesis in hairless mice

S Mikkelsen, B Berne, B Staberg, A Vahlquist

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

Resumé

Vitamin A and its derivatives (retinoids) exert modulatory effects on epithelial differentiation and are used therapeutically against skin cancers, but the role of dietary vitamin A in ultraviolet (UV)-induced carcinogenesis is far from clear. To study this process, 220 hairless mice were given diets containing low (0.3-0.6 mg/kg; A-) or high (4-6 mg/kg; A+) amounts of retinol, which resulted after 2 months in an approximately 4-fold difference in liver and skin vitamin A levels as determined by HPLC. Commencing after 1 month of diet, daily irradiations with UVB (280-320 nm) or UVAB (280-380 nm) were given to 176 of the animals for 18 weeks (cumulative doses of UVB and UVA: 26 J/cm2 and 168 J/cm2, respectively). The first skin tumours, known to be squamous cell carcinomas, appeared after 35 weeks in the UVAB-irradiated A+ animals and 5-6 weeks later in the other groups. After one year the frequency of tumour-bearing animals was 49-63% in the A+ groups and 28-39% in the A- groups (P = 0.003). Two months later the corresponding figures were 66-72% and 50-53%, respectively (P = 0.014). Disregarding the effect of dietary vitamin A, there was no difference in the final tumour incidence between UVB- and UVAB-irradiated animals. The epidermal vitamin A content at 72 h post-irradiation was approximately 60% lower in A+ animals and approximately 10% lower in A- animals compared with the non-irradiated controls. Rather than protecting against skin cancer, a diet rich in vitamin A seems to facilitate UV carcinogenesis in hairless mice. A possible explanation is that photodecomposition of excessive vitamin A generates short-lived intermediates that may act as photosensitizers during cutaneous carcinogenesis.

OriginalsprogEngelsk
TidsskriftCarcinogenesis
Vol/bind19
Udgave nummer4
Sider (fra-til)663-6
Antal sider4
ISSN0143-3334
StatusUdgivet - apr. 1998

Fingeraftryk

Hairless Mouse
Skin Neoplasms
Diet
Skin
Neoplasms
Photosensitizing Agents
High Pressure Liquid Chromatography
Liver
Incidence

Citer dette

Mikkelsen, S., Berne, B., Staberg, B., & Vahlquist, A. (1998). Potentiating effect of dietary vitamin A on photocarcinogenesis in hairless mice. Carcinogenesis, 19(4), 663-6.
Mikkelsen, S ; Berne, B ; Staberg, B ; Vahlquist, A. / Potentiating effect of dietary vitamin A on photocarcinogenesis in hairless mice. I: Carcinogenesis. 1998 ; Bind 19, Nr. 4. s. 663-6.
@article{5083539ceeaa405d85e30f1754557ee4,
title = "Potentiating effect of dietary vitamin A on photocarcinogenesis in hairless mice",
abstract = "Vitamin A and its derivatives (retinoids) exert modulatory effects on epithelial differentiation and are used therapeutically against skin cancers, but the role of dietary vitamin A in ultraviolet (UV)-induced carcinogenesis is far from clear. To study this process, 220 hairless mice were given diets containing low (0.3-0.6 mg/kg; A-) or high (4-6 mg/kg; A+) amounts of retinol, which resulted after 2 months in an approximately 4-fold difference in liver and skin vitamin A levels as determined by HPLC. Commencing after 1 month of diet, daily irradiations with UVB (280-320 nm) or UVAB (280-380 nm) were given to 176 of the animals for 18 weeks (cumulative doses of UVB and UVA: 26 J/cm2 and 168 J/cm2, respectively). The first skin tumours, known to be squamous cell carcinomas, appeared after 35 weeks in the UVAB-irradiated A+ animals and 5-6 weeks later in the other groups. After one year the frequency of tumour-bearing animals was 49-63{\%} in the A+ groups and 28-39{\%} in the A- groups (P = 0.003). Two months later the corresponding figures were 66-72{\%} and 50-53{\%}, respectively (P = 0.014). Disregarding the effect of dietary vitamin A, there was no difference in the final tumour incidence between UVB- and UVAB-irradiated animals. The epidermal vitamin A content at 72 h post-irradiation was approximately 60{\%} lower in A+ animals and approximately 10{\%} lower in A- animals compared with the non-irradiated controls. Rather than protecting against skin cancer, a diet rich in vitamin A seems to facilitate UV carcinogenesis in hairless mice. A possible explanation is that photodecomposition of excessive vitamin A generates short-lived intermediates that may act as photosensitizers during cutaneous carcinogenesis.",
keywords = "Animals, Cocarcinogenesis, Diet, Mice, Mice, Hairless, Neoplasms, Radiation-Induced/etiology, Pilot Projects, Skin/metabolism, Skin Neoplasms/etiology, Vitamin A/administration & dosage",
author = "S Mikkelsen and B Berne and B Staberg and A Vahlquist",
year = "1998",
month = "4",
language = "English",
volume = "19",
pages = "663--6",
journal = "Carcinogenesis",
issn = "0143-3334",
publisher = "Heinemann",
number = "4",

}

Mikkelsen, S, Berne, B, Staberg, B & Vahlquist, A 1998, 'Potentiating effect of dietary vitamin A on photocarcinogenesis in hairless mice', Carcinogenesis, bind 19, nr. 4, s. 663-6.

Potentiating effect of dietary vitamin A on photocarcinogenesis in hairless mice. / Mikkelsen, S; Berne, B; Staberg, B; Vahlquist, A.

I: Carcinogenesis, Bind 19, Nr. 4, 04.1998, s. 663-6.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

TY - JOUR

T1 - Potentiating effect of dietary vitamin A on photocarcinogenesis in hairless mice

AU - Mikkelsen, S

AU - Berne, B

AU - Staberg, B

AU - Vahlquist, A

PY - 1998/4

Y1 - 1998/4

N2 - Vitamin A and its derivatives (retinoids) exert modulatory effects on epithelial differentiation and are used therapeutically against skin cancers, but the role of dietary vitamin A in ultraviolet (UV)-induced carcinogenesis is far from clear. To study this process, 220 hairless mice were given diets containing low (0.3-0.6 mg/kg; A-) or high (4-6 mg/kg; A+) amounts of retinol, which resulted after 2 months in an approximately 4-fold difference in liver and skin vitamin A levels as determined by HPLC. Commencing after 1 month of diet, daily irradiations with UVB (280-320 nm) or UVAB (280-380 nm) were given to 176 of the animals for 18 weeks (cumulative doses of UVB and UVA: 26 J/cm2 and 168 J/cm2, respectively). The first skin tumours, known to be squamous cell carcinomas, appeared after 35 weeks in the UVAB-irradiated A+ animals and 5-6 weeks later in the other groups. After one year the frequency of tumour-bearing animals was 49-63% in the A+ groups and 28-39% in the A- groups (P = 0.003). Two months later the corresponding figures were 66-72% and 50-53%, respectively (P = 0.014). Disregarding the effect of dietary vitamin A, there was no difference in the final tumour incidence between UVB- and UVAB-irradiated animals. The epidermal vitamin A content at 72 h post-irradiation was approximately 60% lower in A+ animals and approximately 10% lower in A- animals compared with the non-irradiated controls. Rather than protecting against skin cancer, a diet rich in vitamin A seems to facilitate UV carcinogenesis in hairless mice. A possible explanation is that photodecomposition of excessive vitamin A generates short-lived intermediates that may act as photosensitizers during cutaneous carcinogenesis.

AB - Vitamin A and its derivatives (retinoids) exert modulatory effects on epithelial differentiation and are used therapeutically against skin cancers, but the role of dietary vitamin A in ultraviolet (UV)-induced carcinogenesis is far from clear. To study this process, 220 hairless mice were given diets containing low (0.3-0.6 mg/kg; A-) or high (4-6 mg/kg; A+) amounts of retinol, which resulted after 2 months in an approximately 4-fold difference in liver and skin vitamin A levels as determined by HPLC. Commencing after 1 month of diet, daily irradiations with UVB (280-320 nm) or UVAB (280-380 nm) were given to 176 of the animals for 18 weeks (cumulative doses of UVB and UVA: 26 J/cm2 and 168 J/cm2, respectively). The first skin tumours, known to be squamous cell carcinomas, appeared after 35 weeks in the UVAB-irradiated A+ animals and 5-6 weeks later in the other groups. After one year the frequency of tumour-bearing animals was 49-63% in the A+ groups and 28-39% in the A- groups (P = 0.003). Two months later the corresponding figures were 66-72% and 50-53%, respectively (P = 0.014). Disregarding the effect of dietary vitamin A, there was no difference in the final tumour incidence between UVB- and UVAB-irradiated animals. The epidermal vitamin A content at 72 h post-irradiation was approximately 60% lower in A+ animals and approximately 10% lower in A- animals compared with the non-irradiated controls. Rather than protecting against skin cancer, a diet rich in vitamin A seems to facilitate UV carcinogenesis in hairless mice. A possible explanation is that photodecomposition of excessive vitamin A generates short-lived intermediates that may act as photosensitizers during cutaneous carcinogenesis.

KW - Animals

KW - Cocarcinogenesis

KW - Diet

KW - Mice

KW - Mice, Hairless

KW - Neoplasms, Radiation-Induced/etiology

KW - Pilot Projects

KW - Skin/metabolism

KW - Skin Neoplasms/etiology

KW - Vitamin A/administration & dosage

M3 - Journal article

VL - 19

SP - 663

EP - 666

JO - Carcinogenesis

JF - Carcinogenesis

SN - 0143-3334

IS - 4

ER -

Mikkelsen S, Berne B, Staberg B, Vahlquist A. Potentiating effect of dietary vitamin A on photocarcinogenesis in hairless mice. Carcinogenesis. 1998 apr;19(4):663-6.