Diets Containing High Levels of Corn Oil Suppress Immunoresponsiveness and Exacerbate UV-Carcinogenesis
Although ultraviolet radiation (UV) is considered a “complete” carcinogen, an irradiation protocol has been devised that approximates the classic two-stage chemical carcinogenesis protocol, allowing inferences to be made as to the segment of the carcinogenic continuum at which dietary lipid exerts its principal effect upon UV-induced skin cancer. Employing this protocol, we have determined that enhancement of UV-carcinogenesis by high levels of polyunsaturated fat (12% corn oil) occurs during the promotion/progression stage; that replacement with a low fat (0.75% corn oil) diet after initiation will negate the exacerbating effect of high fat; and that an omega-3 fatty acid source (12% menhaden oil) inhibits UV-carcinogenesis even at high dietary levels, although apparently exerting its inhibitory effect during UV-initiation. In addition, both dietary lipid sources (corn oil vs. menhaden oil) and level of corn oil markedly influence delayed-type hypersensitivity (DTH) to the hapten, dinitrochlorobenzene. As level of corn oil also influences tumor expression and prostaglandin E2 levels in a near linear fashion and as PGE2 has been reported to modulate immune hypersensitivity responses, we have examined the influence of low/high corn oil levels on DTH during various time intervals within the UV-carcinogenesis protocol. DTH response was significantly (p < 0.01) suppressed in animals receiving high fat diet prior to irradiation. Although both dietary groups exhibited UV-induced immunosuppression, there remained a significant (p = 0.01) difference in response between the dietary groups through nine weeks of irradiation. These data indicate that level of dietary lipid has a pronounced effect upon immunoresponsiveness during carcinogenesis and may partially explain the exacerbation of carcinogenic expression by high corn oil diets.