Comparison of ultraviolet light‐induced skin carcinogenesis and ornithine decarboxylase activity in Sencar and Hairless SKH‐1 mice fed a constant level of dietary lipid varying in corn and coconut oil
- 1 January 1996
- journal article
- other
- Published by Taylor & Francis in Nutrition and Cancer
- Vol. 26 (3) , 353-363
- https://doi.org/10.1080/01635589609514491
Abstract
To investigate the effect of various levels of corn oil and coconut oil on ultraviolet (UV) light‐induced skin tumorigenesis and ornithine decarboxylase (ODC) activity, Sencar and SKH‐1 mice were fed one of three 15% (weight) fat semipurified diets containing three ratios of com oil to coconut oil: 1.0%:14.0%, 7.9%:7.1%, and 15.0%:0.0% in Diets A, B, and C, respectively. Groups of 30 Sencar and SKH‐1 mice were fed one of the diets for three weeks before UV irradiation; then both strains were UV irradiated with an initial dose of 90 mJ/cm2. The dose was given three times a week and increased 25% each week. For Sencar mice (irradiated 33 wks for a total dose of 48 J/cm2), tumor incidence reached a maximum of 60%, 60%, and 53% for Diets A, B, and C, respectively, with an overall average of one to two tumors per tumor‐bearing animal. For the SKH‐1 mice (irradiated 29 wks for a total dose of 18 J/cm2), all diet groups reached 100% incidence by 29 weeks, with approximately 12 tumors per tumor‐bearing mouse. No significant effect of dietary corn oil/coconut oil was found for tumor latency, incidence, or yield in either strain. The effect of increasing com oil on epidermal ODC activity in chronically UV‐irradiated Sencar and SKH‐1 mice was assessed Three groups of mice from each strain were fed one of the experimental diets and UV irradiated for six weeks. Sencar mice showed no increase in ODC activity until six weeks of treatment, when the levels of ODC activity in the UV‐irradiated mice fed Diet A were significantly higher than those in mice fed Diet B or Diet C: 1.27, 0.55, and 0.52 nmol/mg protein/hr, respectively. In the SKH‐1 mice, ODC activity was increased by the first week of UV treatment, and by three weeks of treatment a dietary effect was observed: ODC activity was significantly higher in mice fed Diet C (0.70 nmol/mg protein/hr) than in mice fed Diet A (0.18 nmol/mg protein/hr). Although there was no significant effect of dietary corn oil/coconut oil on UV‐induced tumor incidence, the data indicate that chronically UV‐irradiated hairless SKH‐1 mice are more susceptible to UV‐induced skin carcinogenesis than Sencar mice and that this susceptibility is correlated with increases in ODC activity, a parameter of cell proliferation.Keywords
This publication has 17 references indexed in Scilit:
- Effects of type and amount of dietary fat on mouse skin tumor promotionNutrition and Cancer, 1994
- INFLUENCE OF DIETARY OMEGA‐6, ‐3 FATTY ACID SOURCES ON THE INITIATION AND PROMOTION STAGES OF PHOTOCARCINOGENESISPhotochemistry and Photobiology, 1992
- The effect of the level of dietary corn oil on mouse skin carcinogenesisNutrition and Cancer, 1991
- THE EPIDERMAL CELL KINETIC RESPONSE TO ULTRAVIOLET B IRRADIATION COMBINES REGENERATIVE PROLIFERATION AND CARCINOGEN ASSOCIATED CELL CYCLE DELAYPhotochemistry and Photobiology, 1989
- INFLUENCE OF DIETARY MENHADEN OIL UPON CARCINOGENESIS AND VARIOUS CUTANEOUS REspONSES TO ULTRAVIOLET RADIATION*Photochemistry and Photobiology, 1989
- Photocarcinogenesis and Persistent Hyperplasia in UV-Irradiated SENCAR Mouse SkinEnvironmental Health Perspectives, 1986
- POLYAMINESAnnual Review of Biochemistry, 1984
- DOSE‐TIME DEPENDENCY OF TUMOR FORMATION BY CHRONIC UV EXPOSUREPhotochemistry and Photobiology, 1983
- Influence of dietary lipid upon ultraviolet‐light carcinogenesisNutrition and Cancer, 1983
- Ultraviolet Light Induces Epidermal ornithine Decarboxylase ActivityJournal of Investigative Dermatology, 1978