Diwan B A, Rice J M, Ohshima M, Ward J M, Dove L F
J Natl Cancer Inst. 1985 Feb;74(2):509-16.
Tumor-promoting abilities of four barbiturates, phenobarbital [(PB) CAS: 50-06-6], amobarbital [(AB) CAS: 57-43-2], barbital sodium [(BB) CAS: 144-02-5], and barbituric acid [(BA) CAS: 67-52-7], on the development of neoplasms in livers and other organs of rats following initiation with N-nitrosodiethylamine [(DENA) CAS: 55-18-5] were compared. Four-week-old F344/NCr male rats were given a single ip injection of 75 mg DENA/kg body weight. Beginning 2 weeks later, they were given either tap water (group 1) or drinking water containing 500 ppm of PB (group 2), the sodium salt of BB (group 3), AB (group 4), or BA (group 5) for the remaining experimental period. Control groups (groups 6-10) received an ip injection of saline alone and 2 weeks later were given either tap water or drinking water containing barbiturates as listed above. Animals were sacrificed at either 52 weeks or 78 weeks. None of the barbiturates altered the growth and survival of animals. PB and BB increased liver weights and significantly enhanced the development of hepatocellular foci and hepatocellular adenomas at 52 weeks and hepatocellular foci, hepatocellular adenomas, and trabecular carcinomas at 78 weeks in DENA-treated rats. No such enhancing effects were observed with AB or BA. PB or BB did not significantly enhance the incidence of nonhepatic tumors at 52 weeks. However, at 78 weeks BB significantly enhanced the development of renal tubular adenomas and carcinomas, while PB enhanced the development of thyroid follicular cell neoplasms in DENA-treated rats. These results clearly showed that barbiturates exhibited structure-promoting activity relationships and that their promoting abilities were not restricted to liver alone. Substitution of both hydrogen atoms at the C-5 position of the pyrimidine ring by alkyl or aryl groups appears to be essential but not sufficient for tumor-promoting activity of barbiturates.
比较了四种巴比妥类药物,即苯巴比妥[(PB),化学物质登录号:50 - 06 - 6]、异戊巴比妥[(AB),化学物质登录号:57 - 43 - 2]、巴比妥钠[(BB),化学物质登录号:144 - 02 - 5]和巴比妥酸[(BA),化学物质登录号:67 - 52 - 7],在大鼠经N - 亚硝基二乙胺[(DENA),化学物质登录号:55 - 18 - 5]启动后,对肝脏及其他器官肿瘤发生的促进能力。给4周龄的F344/NCr雄性大鼠腹腔注射一次75 mg DENA/kg体重。2周后开始,在剩余实验期间,它们分别给予自来水(第1组)或含500 ppm PB的饮用水(第2组)、BB的钠盐(第3组)、AB(第4组)或BA(第5组)。对照组(第6 - 10组)仅腹腔注射生理盐水,2周后给予上述含巴比妥类药物的自来水或饮用水。在52周或78周处死动物。所有巴比妥类药物均未改变动物的生长和存活情况。PB和BB增加了肝脏重量,并在52周时显著增强了DENA处理大鼠肝细胞灶和肝细胞腺瘤的发生,在78周时增强了肝细胞灶、肝细胞腺瘤和小梁癌的发生。AB或BA未观察到这种增强作用。PB或BB在52周时未显著提高非肝肿瘤的发生率。然而,在78周时,BB显著增强了DENA处理大鼠肾小管腺瘤和癌的发生,而PB增强了甲状腺滤泡细胞肿瘤的发生。这些结果清楚地表明巴比妥类药物呈现出结构 - 促进活性关系,且它们的促进能力并不局限于肝脏。嘧啶环C - 5位的两个氢原子被烷基或芳基取代似乎对巴比妥类药物的肿瘤促进活性是必要的,但并不充分。