Bradlow H L, Sepkovic D W, Telang N T, Osborne M P
Strang-Cornell Cancer Research Laboratory, New York, New York 10021, USA.
Ann N Y Acad Sci. 1995 Sep 30;768:180-200. doi: 10.1111/j.1749-6632.1995.tb12121.x.
The results show that all of the carcinogens, oncogenes, and tumor-associated viruses that we have studied profoundly affect the extent of 2- and 16 alpha-hydroxylation in a prorisk direction. All of the dietary and biological responses associated with increased cancer risk decrease 2-hydroxylation and increase 16 alpha-hydroxylation. Remarkably, although PAHs are reported to induce P450-1A1, we have found them to decrease 2-hydroxylation. Finally, using indole-3-carbinol to induce 2-hydroxylation results in the chemoprevention of mammary tumors in rodents and recurrences of laryngeal papillomas in humans. Also correlating with these studies in HPV is the decrease in the C-2/C-16 alpha metabolite ratio observed in women with CIN relative to control subjects. The greatest decrease was observed in women with the most severe form, CIN3 (Figure 23). These findings are under further investigation.
结果表明，我们所研究的所有致癌物、致癌基因和肿瘤相关病毒均朝着促癌方向深刻影响2-羟化和16α-羟化的程度。所有与癌症风险增加相关的饮食和生物学反应都会降低2-羟化并增加16α-羟化。值得注意的是，尽管多环芳烃据报道可诱导细胞色素P450-1A1，但我们发现它们会降低2-羟化。最后，使用吲哚-3-甲醇诱导2-羟化可导致啮齿动物乳腺肿瘤的化学预防以及人类喉乳头状瘤的复发。与这些HPV相关研究相关的还有，相对于对照受试者，在患有宫颈上皮内瘤变（CIN）的女性中观察到C-2/C-16α代谢物比率降低。在最严重形式的CIN3女性中观察到最大降幅（图23）。这些发现正在进一步研究中。
