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化学进展 2022, Vol. 34 Issue (10): 2121-2133 DOI: 10.7536/PC220215   后一篇

• 综述与评论 •

环境内分泌干扰物对雌激素受体表达与转录激活的调控效应及分析技术

任志华1,2,4, 杨晓溪1,*(), 孙振东3, 任婧1,2, 桑楠4, 周群芳1,2,3, 江桂斌1,2,3   

  1. 1 中国科学院生态环境研究中心环境化学与生态毒理学国家重点实验室 北京 100085
    2 中国科学院大学资源环境学院 北京 100049
    3 国科大杭州高等研究院环境学院 杭州 310024
    4 山西大学环境与资源学院环境与健康研究中心 太原 030006
  • 收稿日期:2022-02-17 修回日期:2022-03-25 出版日期:2022-10-24 发布日期:2022-04-01
  • 通讯作者: 杨晓溪
  • 基金资助:
    国家重点研发计划(2018YFA0901101); 与国家自然科学基金项目(22193050); 与国家自然科学基金项目(22176203); 与国家自然科学基金项目(21906180); 与国家自然科学基金项目(22276212)
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Regulation of Environmental Endocrine Disrupting Chemicals on the Expressions and Transactivation of Estrogen Receptors and the Related Analytical Techniques

Ren Zhihua1,2,4, Yang Xiaoxi1(), Sun Zhendong3, Ren Jing1,2, Sang Nan4, Zhou Qunfang1,2,3, Jiang Guibin1,2,3   

  1. 1 State Key Laboratory of Environmental Chemistry and Ecotoxicology, Research Center for Eco-Environment, Chinese Academy of Sciences, Beijing 100085, China
    2 College of Resources and Environment, University of Chinese of Academy of Sciences, Beijing 100049, China
    3 School of Environment, Hangzhou Institute for Advanced Study, University of Chinese Academy of Sciences, Hangzhou 310024, China
    4 College of Environment and Resource, Research Center of Environment and Health, Shanxi University, Taiyuan 030006, China
  • Received:2022-02-17 Revised:2022-03-25 Online:2022-10-24 Published:2022-04-01
  • Contact: Yang Xiaoxi
  • Supported by:
    National Key R&D Program of China(2018YFA0901101); National Natural Science Foundation of China(22193050); National Natural Science Foundation of China(22176203); National Natural Science Foundation of China(21906180); National Natural Science Foundation of China(22276212)

环境内分泌干扰物(Endocrine disrupting chemicals, EDCs)种类繁多,来源复杂,环境污染普遍,对野生动物与人类造成了不同程度的暴露。EDCs可通过调控机体内分泌系统,干扰心血管、生殖、神经等多个系统的正常功能,从而引起机体代谢综合征、肥胖症、神经毒性、生殖发育毒性和癌症等的发生发展。污染物调控雌激素受体(Estrogen receptors, ERs)产生内分泌干扰效应是当前EDCs研究的主要方向。本文围绕ERs的基本生理特征、ERs表达与转录激活的分析检测技术,及EDCs调控不同组织来源ERs的生物学意义进行系统综述,以期从ERs激动/拮抗效应的角度,为新型化学品的内分泌干扰效应筛选及分子机制解析提供科学思路。

关键词： 新型污染物, 内分泌干扰效应, 雌激素受体, 不同种属, 转录激活

An increasing number of chemicals with endocrine disrupting effects, such as environmental endocrine disrupting chemicals (EDCs), have been emerging in the environment. Diverse molecules, such as natural chemicals existing in food and synthetic chemicals used in daily products, are identified as endocrine disruptors. With the inevitable release of EDCs, these chemicals are found to be distributed in various environmental matrixes including water, soil and sediments, posing a threat to wildlife and humans. The universal contamination of EDCs may disturb the endocrine system of the wildlife and human beings, potentially causing toxicological effects on multiple targets, like cardiovascular, reproductive and nervous systems, and probably inducing the incidence of metabolic syndrome, obesity, neurological disorder, reproductive and developmental toxicity, and even cancer. Among investigations about mechanisms underlying endocrine disrupting effect, the estrogen receptors (ERs) mediated pathway is one of the hotly-discussed aspects in EDC studies. In this review, the basic characteristics of ERs, analytical techniques for ERs expression and transactivation, and biological significance of EDCs via the regulation of ERs in different organisms were systemically introduced, intending to provide promising strategies for screening the endocrine disrupting effects of emerging chemicals of concern and evaluating their hazardous risks from the aspects of ERs agonistic and antagonistic activities.

Key words: emerging chemicals of concern, endocrine disrupting effects, estrogen receptors, different species, transactivation
()
图1 ER信号通路
Fig. 1 ER signaling pathways
表1 内分泌干扰物通过ERs调控的生物学效应
Table 1 The biological effects of EDCs mediated by ERs
Type Chemical Species ER-mediated signaling Biological response ref
Endogenous estrogen E2 Mouse prostate mesenchyme cells ERα expression Growth induction, increase in health risk of prostate size enlargement 65
MCF-7, T47D, MDA-MB-231 cells ERs Increase in cell proliferation 104
T47D cells ERβ Decrease in proliferation through affecting cell-cycle machinery 108
HepG2 cells ERα36, ERα66 and ERβ expression Testosterone-induced cell proliferation inhibition 89
MCF-7 BUS cells ERs expressions Increase in cell proliferation 110
Mussels (Mytilus edulis) ERs expression VTG induction, gametogenesis process disorder 67
SD female rats ERβ Arrhythmia and sarcoplasmic reticulum calcium handling promotion 80
Mice ERα Increase in insulin biosynthesis and β-cell exhaustion 87,88
Synthetic estrogen EE2 Mussels (Mytilus edulis) ERs expression VTG induction, gametogenesis process disorder 67
Zebrafish ERβ Primordial germ cell migration and distribution disruption 57
C57 BL/6 mice ERα Hepatotoxicity including repression of hepatic transporters and alterations of bile acid biosynthesis 100
SD male rats Liver cytosolic ERα Endocrine system disruption 90
Phyto-
estrogens		 Genistein MCF-7 cells ER Increase in cell proliferation, activation of estrogen-responsive gene TFF1 105
Genistein and Resveratrol MCF-7 cells ERs binding and expressions Cell growth stimulation, activation of estrogen-responsive gene TFF1 109
SD female rats Liver cytosolic ERα Endocrine system disruption 90
SD male rats Liver cytosolic ERα Endocrine system disruption 90
Human and mice ER binding Specific cancers chemoprevention 114
Pesticides and
herbicides		 Chlordecone Rainbow trout hepatocytes ER VTG induction 93
Chlorpyriphos MCF-7 BUS cells ERs expression Increase in cell proliferation 110
Methoxychlor Zebrafish embryos and larvae ER Hatching delay, increase in mortality rate and VTG induction 94
Chlorane Green neon shrimps ER Male, morphological alterations of masculine appendage, testosterone reduction; Female, increase in estrogen, reproduction obstacles 59,60
GBHs Wistar rats ERα expression Mammary gland development alteration in male 111
Phenolic
compounds		 BPA Mouse prostate mesenchyme cells ERα expression Growth induction, increase in the risk of prostate size enlargement 65
SH-SY5Y cells ERα activation Increase in cell proliferation, invasion and migration 113
Nonylphenols Zebrafish embryos and larvae ER Hatching delay, increase in mortality rate, VTG induction 94
4-Hexylphenol SD female rats Hypothalamus ERα expression Neuroendocrine system disruption 75
SD female rat ERβ Arrhythmia and sarcoplasmic reticulum calcium handling promotion 80
Mice ERα Increase in insulin biosynthesis and β-cell exhaustion 87,88
Human and mice ER Correlation with the incidence of estrogen-dependent cancers 114
Mice ERs Neurodevelopmental impairment, behavioral disorders 70
Rainbow trout hepatocytes ER VTG induction 93
SH-SY5Y cells ERα activation Increase in cell proliferation, invasion and migration 113
Mice ER Increase in secretion of TNF-α and IL-1β in the liver 99
3T3-L1 cells ERs Adipogenic differentiation promotion 86
HepG2 cells ERs Hepatic lipid accumulation 86
Organic halogen compounds PFOS, PFOA Human and rainbow trout ER VTG induction 96
PFBDI, PFHxDI Primary cultured tilapia hepatocytes ER VTG induction 95
PFOI Zebrafish embryos ERα and estrogenic synthesis genes expression Estradiol production alteration 97
PFOS
HBCD Adult male Japanese medaka Hepatic ER VTG induction 32
TBBPA Male C57 mice Testicular ERα and ERβ expressions Serum testosterone reduction, decrease in proliferation of germ cells, increase in apoptosis of germ cells 68
Aroclor 1245
Mice ERβ Hydropic degeneration, vacuolation induction, and reduction in bile acid and cholesterol levels 115
MCF-7 cells ER Increase in cell proliferation, activation of estrogen-responsive gene TFF1 107
Zebrafish embryos and larvae ER Hatching delay, increase in mortality rate, VTG induction 94
Rainbow trout hepatocytes ER VTG induction 93
Aroclor 1221 SD rats AVPV ERβ Permanent impairment in brain structure and function 76
Dioxins Human and mice ER Correlation with the incidence of estrogen-dependent cancers 114
Phthalates DBP, DINP Zebrafish embryos ERα and ERβa expression
ERβb expression		 Brain size and number of proliferating neurons reduction 73
DEHP Human and mice ER Correlation with the incidence of estrogen-dependent cancers 114
PAHs D4 C57BL/6 mice Brain ERα and ERβ expression Cell cycle progression of neuronal progenitor cells alteration, cognitive dysfunction, memory reduction and motor learning defect 74
Benzo[a]pyrene Wistar rats ERα Increase in uterine weight, hypertrophy of luminal epithelium 61
Parabens Methylparaben MCF-7 cells ER binding, ERα expression Increase in cell proliferation 106
Triazole fungicides Tebuconazole Cyproconazole HepG2 cells ERα transactivation Increase in estrogen synthesis and secretion, metabolism of macromolecules disruption 92
Furan Furan B3C6F1 mice Liver ERα expression Interference with stress-activated protein kinase, death receptor, ERKs and TNF-α pathways 91
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