Mei J J, Hursting S D, Perkins S N, Phang J M
Laboratory of Nutritional and Molecular Regulation, Division of Basic Sciences, National Cancer Institute, Frederick, MD 21702-1201, USA.
Cancer Lett. 1998 Jul 17;129(2):191-7. doi: 10.1016/s0304-3835(98)00102-5.
We have previously reported that dietary interventions with purported anti-inflammatory activity delay spontaneous tumorigenesis in p53-deficient (p53-/-) mice. In the present study, 4 weeks of calorie restriction or the dietary administration of chemopreventive steroids dehydroepiandrosterone and 16alpha-fluoro-5-androsten-17-one significantly reduced the inducible generation of nitric oxide (NO) in ex vivo peritoneal macrophages from male p53 wild-type and p53-/- mice relative to the respective ad libitum-fed controls; expression of inducible nitric oxide synthase II (NOS2) protein was also markedly decreased compared with respective controls. These findings suggest that the p53-independent suppression of inducible NO production observed in this study may contribute to the anti-cancer effects of these preventive interventions in p53-/- mice.
我们之前曾报道，具有所谓抗炎活性的饮食干预可延缓p53基因缺陷（p53-/-）小鼠的自发肿瘤发生。在本研究中，与各自自由进食的对照组相比，4周的热量限制或饮食给予化学预防类固醇脱氢表雄酮和16α-氟-5-雄烯-17-酮可显著降低雄性p53野生型和p53-/-小鼠离体腹膜巨噬细胞中一氧化氮（NO）的诱导生成；与各自的对照组相比，诱导型一氧化氮合酶II（NOS2）蛋白的表达也显著降低。这些发现表明，本研究中观察到的p53非依赖性诱导型NO生成抑制可能有助于这些预防干预措施对p53-/-小鼠的抗癌作用。
