Lack of rapid initiating, promoting or sequential syncarcinogenic effects of di(2-ethylhexyl)phthalate in rat liver carcinogenesis.
Lack of rapid initiating, promoting or sequential syncarcinogenic effects of di(2-ethylhexyl)phthalate in rat liver carcinogenesis.
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邻苯二甲酸二(2-乙基己基)酯在大鼠肝癌发生中缺乏快速引发、促进或序贯致癌作用。
DOI：
10.1093/carcin/8.7.875
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发表时间：
1987
期刊：
影响因子：
4.7
通讯作者：
Tanaka,T
中科院分区：
文献类型：
--
作者：
Williams,GM;Maruyama,H;Tanaka,T
研究了长期饮食摄入过氧化物酶增殖剂邻苯二甲酸二(2-乙基己基)酯(DEHP)对BYN-2-氟甲基二甲胺(FAA)和促癌剂苯巴比妥(PB)诱发小鼠肝癌的影响。此外，还研究了DEHP作为引发剂的作用，它取代了PB之前的FAA。雄性大鼠喂饲FAA 7周以诱导肝细胞病变，随后不给予任何化学物质，每分钟12,000次。DEHP或下午500PB在饮食中持续24周。在饲喂DEHP的大鼠，肝实质肿大和过氧化物酶的增殖。单独给药24周或7周后加用PB均未发现肝细胞变性灶或肝肿瘤形成的证据。此外，饲喂24周的DEHP对FAA诱导的肝脏改变灶没有促进作用，对FAA诱导的肝肿瘤的发生几乎没有促进作用。相比之下，PB对病灶有明显的增强作用，显著增加了肝肿瘤的发生率和多发性。因此，这些发现表明，DEHP既没有快速启动活性，也没有显著的顺序致癌活性，也没有促进肝癌发生的作用，在已确定的许多具有此类活性的试剂的条件下。
The effect of prolonged dietary administration of the peroxisome proliferating plasticizer di(2-ethylhexy1)phthalate (DEHP was studied on liver carcinogenesis initiated byN-2- fltuorenylmxhmide (FAA) and with that of the neoplasm-promoter phenobarbital (PB). Also, DEHP was studied as an initiator by giving it in place of FAA before PB. Male rats were fed FAA for 7 weeks to induce bepatocellular altered foci, and were subsequently given no chemical, 12 000 p.p.m. DEHP or 500 p.p.m. PB for 24 weeks in the diet. In the rats fed DEHP, substantial hepatomegaly and peroxisome proliferation were induced. No evidence of indudion of hepatacellular altered foci or hepatic neoplasms was found either when DEHP was given alone for 24 weeks or for 7 weeks followed by PB. Also, DEHP fed for 24 weeks had no promoting effect on liver altered foci that were induced by FAA and produced little or no enhancement of the occurrence of FAA-induced liver neoplasms. In contrast, PB exerted a marked enhancing effect on foci and substantially increased the incidence and multiplicity of liver neoplasms. Thus, the findings demonstrate that DEHP did not have either a rapid initiating activity, a significant sequential syncarcinogenic activity, or a promoting effect on liver carcinogenesis under conditions in which numerous agents with such activities have been identified.