Hirose M, Inoue T, Asamoto M, Tagawa Y, Ito N
Carcinogenesis. 1986 Aug;7(8):1285-9. doi: 10.1093/carcin/7.8.1285.
Groups of 6-week-old male Syrian golden hamsters were given 13 different phenolic compounds for 20 weeks. Of these compounds, 2(3)-tert-butyl-4-methoxyphenol (BHA), 2-tert-butyl-4-methylphenol (TBMP) and p-tert-butylphenol (PTBP) strongly induced hyperplasia and tumorous lesions in the forestomach. Catechol, p-methylphenol (PMYP), p-methoxyphenol (PMOP), caffeic acid, methylhydroquinone (MHQ) and pyrogallol were less active, and resorcinol, hydroquinone, propylparabene and tert-butylhydroquinone (TBHQ) were not active. The labelling index in the forestomach epithelium was significantly increased by addition to the diet of BHA, TBMP, catechol, PMOP, PTBP and MHQ. PMOP induced epithelial damage and regenerative hyperplasia of the pyloric region. Catechol, caffeic acid and PMYP induced similar though less marked lesions. The labelling index in the glandular stomach was significantly increased by oral catechol (P less than 0.05) or PMOP (P less than 0.05). No histopathological lesions were observed in the urinary bladder epithelium, but propylparabene (P less than 0.05), catechol, TBHQ and MHQ increased the labeling index. These findings indicate that PTBP and TBMP may be carcinogenic for hamster forestomach after long-term administration, and that both one hydroxy and tert-butyl substituents may be important for induction of hamster forestomach tumors.
将6周龄的雄性叙利亚金黄地鼠分成几组,给它们喂食13种不同的酚类化合物,持续20周。在这些化合物中,2(3)-叔丁基-4-甲氧基苯酚(丁基羟基茴香醚,BHA)、2-叔丁基-4-甲基苯酚(TBMP)和对叔丁基苯酚(PTBP)强烈诱导前胃增生和肿瘤性病变。儿茶酚、对甲基苯酚(PMYP)、对甲氧基苯酚(PMOP)、咖啡酸、甲基对苯二酚(MHQ)和连苯三酚的活性较低,而间苯二酚、对苯二酚、尼泊金丙酯和叔丁基对苯二酚(TBHQ)则无活性。在饮食中添加BHA、TBMP、儿茶酚、PMOP、PTBP和MHQ可显著提高前胃上皮的标记指数。PMOP诱导幽门区域上皮损伤和再生性增生。儿茶酚、咖啡酸和PMYP诱导了类似但不太明显的病变。口服儿茶酚(P<0.05)或PMOP(P<0.05)可显著提高腺胃的标记指数。膀胱上皮未观察到组织病理学病变,但尼泊金丙酯(P<0.05)、儿茶酚、TBHQ和MHQ增加了标记指数。这些发现表明,长期给药后,PTBP和TBMP可能对仓鼠前胃具有致癌性,并且一个羟基和叔丁基取代基对于诱导仓鼠前胃肿瘤可能都很重要。