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

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 corn 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 corn 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 increased in ODC activity, a parameter of cell proliferation.

Dietary lipid varying in corn and coconut oil influences protein Kinase C in phorbol ester‐treated mouse skin

“…After one month on the diets (i.e., the mice were then 8 wk of age) the average body weights of mice fed Diets L, M, and H were 38.0 ± 1.4,40.8 + 3.9, and 39.5 ± 0.7 (SD) g, respectively. There were thus no significant differences in body weight between the diet groups in the study, and this is corroborated by the results of an earlier study using the same diets fed to Sencar mice (24).…”

“…The role of linoleate in phorbol ester-induced skin tumor promotion has been of interest, because it is the substrate for the synthesis of arachidonate and also because it can compete with arachidonate for incorporation into the ín-2-position of phospholipids and for lipoxygenase metabolism, which gives rise to hydroxy derivatives, which have been shown to modulate proliferation and differentiation (23). Phosphatidylcholine linoleate was increased in mice fed the 7.9% and 15.0% corn oil diets compared with animals fed the 1.0% corn oil diet; phosphatidylcholine arachidonate remained the same or decreased slightly as dietary corn oil increased (24).…”

The hairless mouse in skin research

“…SKH1 mice are highly susceptible to UVR induced skin cancer [77]; this susceptibility may be a function of the hairless gene itself, as C3H hairless mice are more susceptible to UVR carcinogenesis than haired mice of the same strain [78]. The SKH1 hairless mouse develops lesions resembling UVR-induced tumors in man and can be employed in studies that yield quantitative data suitable for both mechanistic studies and risk assessment purposes.…”

UVB Irradiation-induced Activator Protein-1 Activation Correlates with Increased c-fos Gene Expression in a Human Keratinocyte Cell Line

“…It has also been shown that UVB irradiation leads to cell proliferation in vivo (12). The consequent effect of UVBinduced cell proliferation might lead to tumorigenesis (13). Huang et al (14) reported that UVB irradiation induced AP-1 transactivation in a mouse epithelial cell line.…”