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Promoting activity of di(2-ethylhexyl)phthalate in rat liver foci bioassay.邻苯二甲酸二（2-乙基己基）酯在大鼠肝脏病灶生物测定中的促癌活性。
J Cancer Res Clin Oncol. 1988;114(2):133-6. doi: 10.1007/BF00417826.
2
Di-n-octyl phthalate (DOP), a relatively ineffective peroxisome inducing straight chain isomer of the environmental contaminant di(2-ethylhexyl)phthalate (DEHP), enhances the development of putative preneoplastic lesions in rat liver.邻苯二甲酸二辛酯（DOP）是环境污染物邻苯二甲酸二（2-乙基己基）酯（DEHP）的一种诱导过氧化物酶体效果相对较差的直链异构体，它能促进大鼠肝脏中假定的癌前病变的发展。
Toxicology. 1986 Nov;41(3):279-88. doi: 10.1016/0300-483x(86)90182-4.
3
Inhaled ethylene oxide induces preneoplastic foci in rat liver.吸入环氧乙烷可诱导大鼠肝脏产生癌前病灶。
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Dietary effects on initiation and promotion of hepatocarcinogenesis in rat.饮食对大鼠肝癌发生起始和促进阶段的影响。
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Phosphorylation of specific rat plasma membrane proteins during promotion of gamma-glutamyl transpeptidase-positive hepatic foci and inhibition by di(2-ethylhexyl)phthalate.γ-谷氨酰转肽酶阳性肝灶促进过程中大鼠特定质膜蛋白的磷酸化及邻苯二甲酸二（2-乙基己基）酯的抑制作用
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Di(2-ethylhexyl)phthalate alters carbohydrate enzyme activities and foci incidence in rat liver.邻苯二甲酸二（2-乙基己基）酯改变大鼠肝脏中的碳水化合物酶活性和病灶发生率。
Carcinogenesis. 1990 Dec;11(12):2111-5. doi: 10.1093/carcin/11.12.2111.
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Lack of hepatic promotional activity by the peroxisomal proliferating hepatocarcinogen di(2-ethylhexyl)phthalate.过氧化物酶体增殖性肝癌致癌物邻苯二甲酸二（2-乙基己基）酯缺乏肝脏促癌活性。
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Dissimilar patterns of promotion by di(2-ethylhexyl)phthalate and phenobarbital of hepatocellular neoplasia initiated by diethylnitrosamine in B6C3F1 mice.邻苯二甲酸二（2-乙基己基）酯和苯巴比妥对二乙基亚硝胺引发的B6C3F1小鼠肝细胞瘤的不同促进模式。
Carcinogenesis. 1983 Aug;4(8):1021-9. doi: 10.1093/carcin/4.8.1021.

引用本文的文献

1
Modes of action and species-specific effects of di-(2-ethylhexyl)phthalate in the liver.邻苯二甲酸二（2-乙基己基）酯在肝脏中的作用模式及物种特异性效应
Crit Rev Toxicol. 2006 May;36(5):459-79. doi: 10.1080/10408440600779065.

本文引用的文献

1
Carcinogenesis Bioassay of Di(2-ethylhexyl)phthalate (CAS No. 117-81-7) in F344 Rats and B6C3F1 Mice (Feed Studies).邻苯二甲酸二（2-乙基己基）酯（CAS编号：117-81-7）在F344大鼠和B6C3F1小鼠中的致癌生物测定（饲料研究）
Natl Toxicol Program Tech Rep Ser. 1982 Mar;217:1-127.
2
The carcinogenicity of dietary di(2-ethylhexyl) phthalate (DEHP) in Fischer 344 rats and B6C3F1 mice.膳食邻苯二甲酸二（2-乙基己基）酯（DEHP）对费希尔344大鼠和B6C3F1小鼠的致癌性。
J Toxicol Environ Health. 1982 Oct-Nov;10(4-5):797-815. doi: 10.1080/15287398209530296.
3
Dissimilar patterns of promotion by di(2-ethylhexyl)phthalate and phenobarbital of hepatocellular neoplasia initiated by diethylnitrosamine in B6C3F1 mice.邻苯二甲酸二（2-乙基己基）酯和苯巴比妥对二乙基亚硝胺引发的B6C3F1小鼠肝细胞瘤的不同促进模式。
Carcinogenesis. 1983 Aug;4(8):1021-9. doi: 10.1093/carcin/4.8.1021.
4
Di(2-ethylhexyl) phthalate.
IARC Monogr Eval Carcinog Risk Chem Hum. 1982 May;29:269-94.
5
Investigation of the potential for binding of Di(2-ethylhexyl) phthalate (DEHP) and Di(2-ethylhexyl) adipate (DEHA) to liver DNA in vivo.邻苯二甲酸二（2-乙基己基）酯（DEHP）和己二酸二（2-乙基己基）酯（DEHA）在体内与肝脏DNA结合潜力的研究。
Toxicol Appl Pharmacol. 1984 May;73(3):373-87. doi: 10.1016/0041-008x(84)90089-9.
6
Inhibition of development of preneoplastic lesions in the livers of rats fed a weakly carcinogenic environmental contaminant.对喂食弱致癌性环境污染物的大鼠肝脏中癌前病变发展的抑制作用。
Cancer Lett. 1983 Sep;20(2):199-205. doi: 10.1016/0304-3835(83)90049-6.
7
Sequential histologic study of rat liver during peroxisome proliferator [4-chloro-6-(2,3-xylidino)-2-pyrimidinylthio]-acetic acid (Wy-14,643)-induced carcinogenesis.在过氧化物酶体增殖剂[4-氯-6-(2,3-二甲苯胺基)-2-嘧啶硫基]乙酸（Wy-14,643）诱导的大鼠肝脏致癌过程中的连续组织学研究。
J Natl Cancer Inst. 1984 Oct;73(4):983-90.
8
Di(2-ethylhexyl)phthalate but not phenobarbital promotes N-nitrosodiethylamine-initiated hepatocellular proliferative lesions after short-term exposure in male B6C3F1 mice.
Cancer Lett. 1984 Aug;24(1):49-55. doi: 10.1016/0304-3835(84)90079-x.
9
Lack of genotoxic activity of di(2-ethylhexyl)phthalate (DEHP) in rat and human hepatocytes.邻苯二甲酸二（2-乙基己基）酯（DEHP）在大鼠和人肝细胞中无基因毒性活性。
Carcinogenesis. 1984 Oct;5(10):1329-35. doi: 10.1093/carcin/5.10.1329.
10
Promoting effect of polychlorinated biphenyls on development of enzyme-altered islands in livers of weanling and adult rats.多氯联苯对断奶大鼠和成年大鼠肝脏中酶改变岛形成的促进作用。
J Cancer Res Clin Oncol. 1983;105(2):141-7. doi: 10.1007/BF00406924.

邻苯二甲酸二（2-乙基己基）酯在大鼠肝脏病灶生物测定中的促癌活性。

Promoting activity of di(2-ethylhexyl)phthalate in rat liver foci bioassay.

作者信息

Oesterle D, Deml E

机构信息

Gesellschaft für Strahlen- und Umweltforschung, Neuherberg, Federal Republic of Germany.

出版信息

J Cancer Res Clin Oncol. 1988;114(2):133-6. doi: 10.1007/BF00417826.

DOI:10.1007/BF00417826
PMID:2895111
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12243784/
Abstract

The plasticizer DEHP but not DEHS exerted a weak promoting effect in a 12-week rat liver foci bioassay, using weanling female Sprague-Dawley rats. The effect was similar after doses of 200 and 500 mg/kg body weight, given 3 times weekly by gavage for 11 consecutive weeks after initiation with a single oral dose of 8 mg DEN/kg body weight. Lower doses were ineffective. The incidence of foci with deficiency in ATPase was enhanced about twice compared to rats treated with DEN only. The incidence of foci with expression of GGTase was not affected by DEHP treatment. The results match the findings with lifetime exposure studies, when liver tumors were found in rats and mice. The actual risk for man from environmental DEHP contamination seems to be low; the intake from highly contaminated food is calculated to be about 400-fold lower than the lowest effective dose in this study.

摘要

在一项为期12周的大鼠肝脏病灶生物测定中，增塑剂邻苯二甲酸二（2-乙基己基）酯（DEHP）而非邻苯二甲酸二乙酯（DEHS）对断奶雌性斯普拉格-道利大鼠产生了微弱的促进作用。在以8毫克/千克体重的剂量单次口服给予二乙基亚硝胺（DEN）启动后，连续11周每周3次通过灌胃给予200和500毫克/千克体重的剂量，效果相似。较低剂量无效。与仅用DEN处理的大鼠相比，ATP酶缺乏的病灶发生率提高了约两倍。GGT酶表达的病灶发生率不受DEHP处理的影响。这些结果与终生暴露研究的结果相符，在该研究中大鼠和小鼠出现了肝脏肿瘤。人类因环境中DEHP污染而面临的实际风险似乎较低；据计算，从高度污染食物中的摄入量比本研究中的最低有效剂量低约400倍。