Reeve V E, Bosnic M, Boehm-Wilcox C
Department of Veterinary Pathology, University of Sydney, NSW, Australia.
Cancer Lett. 1996 Nov 29;108(2):271-9. doi: 10.1016/s0304-3835(96)04460-6.
A series of semi-purified diets containing 20% fat by weight, of increasing proportions (0, 5%, 10%, 15% or 20%) of polyunsaturated sunflower oil mixed with hydrogenated saturated cottonseed oil, was fed to groups of Skh:HR-1 hairless mice during induction and promotion of photocarcinogenesis. The photocarcinogenic response was of increasing severity as the polyunsaturated content of the mixed dietary fat was increased, whether measured as tumour incidence, tumour multiplicity, progression of benign tumours to squamous cell carcinoma, or reduced survival. At the termination of the study approximately 6 months following the completion of the 10-week chronic UV irradiation treatment, when most mice bore tumours, the contact hypersensitivity (CHS) reactions in those groups supporting the highest tumour leads (fed 15% or 20% polyunsaturated fat), were significantly suppressed in comparison with the mice bearing smaller tumour loads (fed 0, 5% or 10% polyunsaturated fat). When mice were exposed acutely to UV radiation (UVR), a diet of 20% saturated fat provided almost complete protection from the suppression of CHS, whereas feeding 20% polyunsaturated fat resulted in 57% suppression; the CHS of unirradiated mice was unaffected by the nature of the dietary fat. These results suggest that the enhancement of photocarcinogenesis by the dietary polyunsaturated fat component is mediated by an induced predisposition to persistent immunosuppression caused by the chronic UV irradiation, and supports the evidence for an immunological role in dietary fat modulation of photocarcinogenesis in mice.
在光致癌作用的诱导和促进阶段，将一系列按重量计含20%脂肪的半纯化饮食喂给几组Skh:HR-1无毛小鼠，这些饮食中多不饱和向日葵油与氢化饱和棉籽油的比例逐渐增加（0%、5%、10%、15%或20%）。无论以肿瘤发生率、肿瘤多发性、良性肿瘤向鳞状细胞癌的进展或生存率降低来衡量，随着混合膳食脂肪中多不饱和成分的增加，光致癌反应的严重程度也在增加。在为期10周的慢性紫外线照射治疗结束约6个月后研究终止时，当大多数小鼠患有肿瘤时，与肿瘤负荷较小的小鼠（喂食0%、5%或10%多不饱和脂肪）相比，那些肿瘤发生率最高的组（喂食15%或20%多不饱和脂肪）的接触性超敏反应（CHS）受到显著抑制。当小鼠急性暴露于紫外线辐射（UVR）时，20%饱和脂肪的饮食几乎能完全保护小鼠免受CHS抑制，而喂食20%多不饱和脂肪则导致57%的抑制；未照射小鼠的CHS不受膳食脂肪性质的影响。这些结果表明，膳食多不饱和脂肪成分对光致癌作用的增强是由慢性紫外线照射诱导的对持续性免疫抑制的易感性介导的，并支持了膳食脂肪在小鼠光致癌作用调节中具有免疫作用的证据。
