水中典型环境雌激素共存对内分泌系统的影响及机制研究
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摘要
我国饮用水水源污染严重,其中环境雌激素的污染尤为重要,由于环境雌激素危害大,去除效果差,已引起广泛关注。环境雌激素多以混合状态存在,且无论在环境还是在生物体内均与天然雌激素雌二醇(E2)共同发挥作用。因此对于饮用水中多种典型环境雌激素与E2共存时的活性研究具有非常重要的实际意义。
本论文选取原水中典型环境雌激素双酚A(BPA)、壬基酚(NP)、邻苯二甲酸二丁酯(DBP)、镉(Cd)和六氯苯(HCB)与雌二醇(E2)混合后进行试验,由于以上五种化合物的来源不同,具有不同的生物活性,同时通过不同的作用机制发挥雌激素活性,因此用于研究与E2混合后的雌激素活性变化具有代表性。首先利用细胞增殖实验对以上环境雌激素进行活性测定,确定量效关系。从结果可知,选取的环境雌激素均能诱导细胞增殖,E2引起雌激素效应的剂量最小,HCB诱导的雌激素效应最强,所有环境雌激素的剂量效应关系都符合抛物线形状。E2、BPA、NP在48h诱导细胞增殖的效应最强,DBP、Cd、HCB在72h诱导细胞增殖的效应最强,DBP、Cd、HCB具有效应累积性,雌激素活性的发挥有时间差别。根据单一环境雌激素检测结果,测定以上环境雌激素与E2混合后的活性变化。结果表明:E2与其他单一及混合环境雌激素联合作用时,主要发挥了弱化作用,减弱了其他单一及混合环境雌激素的雌激素效应。
为了阐明环境雌激素与E2混合后的活性变化,进行了混合活性的机制研究。结果表明:E2与其他环境雌激素联合作用于乳腺癌MCF-7细胞48h,E2对BPA、DBP、Cd、HCB发生弱化作用,但与NP却发生了协同作用。针对E2对其他环境雌激素的这种影响,分别从雌激素受体和丝裂原活化蛋白激酶(MAPK)信号通路的角度进行研究,进而确定联合前后的机制变化。研究发现E2、NP、DBP、Cd和HCB都可以通过雌激素受体和胞外信号调节激酶(ERK)信号途径诱导细胞增殖,而BPA通过受体途径发挥作用。BPA、NP、DBP、Cd和HCB分别与E2混合后,都可以通过雌激素受体和ERK信号途径,激活不同的转录因子,诱导细胞增殖。
同时开展了环境雌激素与E2混合后对大鼠睾丸支持细胞的影响研究。利用细胞增殖试验检测E2与BPA、NP、DBP、Cd、HCB混合后对睾丸支持细胞的影响,以上化合物单独作用时,Cd抑制了细胞的增殖,其他化合物促进了细胞的增殖,联合后均能诱导支持细胞的增殖,但增殖程度不一致,因此对影响机制进行研究,发现E2通过周期调控的机制影响了睾丸支持细胞的增殖;BPA通过激活ERK信号通路诱导增殖,与E2联合后机制不变;NP、DBP通过c-Jun氨基末端激酶(JNK)信号通路发挥的作用,与E2联合后这种JNK通路依然发挥作用;Cd通过抑制p-ERK蛋白发挥抑制作用,与E2联合后,抑制作用消失;HCB是通过激活了JNK信号通路诱导细胞增殖,与E2联合组是通过抑制p-ERK而发挥抑制作用。
研究环境雌激素与E2混合后的活性,最终是要对饮用水的雌激素活性进行分析,保障饮用水的安全。对原水、沉后水、滤后水、出厂水及管网水的雌激素活性及其作用机制进行研究。结果表明各处理工艺能够有效的降低原水的雌激素活性,随着处理工艺的深入,活性降低。出厂水雌激素活性消失,但管网水较出厂水雌激素活性稍有增高,表明在管网运输过程中发生了物理化学变化,改变了水中环境雌激素的性质。饮用水各处理工艺出水对睾丸支持细胞的影响同样是研究的重点,研究结果表明,原水能够促进睾丸支持细胞增殖,随着处理工艺的深入,其他单元出水对睾丸支持细胞几乎没有影响,说明水处理工艺能够有效的降低环境雌激素的生物活性。在此基础上,对饮用水各处理工艺出水内分泌干扰的机制进行研究,结果表明:对乳腺癌MCF-7细胞的影响机制为,原水、滤后水和出厂水通过雌激素受体途径和p-ERK信号通路激活核内转录因子c-Myc蛋白和c-Fos基因发挥增殖作用,而沉后水、管网水可以通过雌激素受体通路和ERK信号通路诱导c-Myc蛋白表达进而促进细胞增殖。滤后水还可以通过c-Jun基因的激活诱导增殖。对睾丸支持细胞影响的机制为,原水通过激活p-JNK信号通路,诱导cyclinD1蛋白表达,抑制了细胞的凋亡进而增加了细胞的数量,而其他各处理工艺出水中环境雌激素含量减少,因此对蛋白诱导的能力降低,没有诱导支持细胞增殖。
The serious source water pollution in China, especially the pollution by environmental estrogens, has caused widespread concerns. The environmental estrogens are of great health hazards and are hard to be removed. Environmental estrogens mainly exist as mixtures and function together with E2 in the environment and in vivo. So it is of important practical significance to study the activity when multiple environmental estrogens coexist with E2.
Six typical estrogens in water source were selected, namely E2, BPA, NP, DBP, Cd, and HCB. These estrogens are of different sources, have different biological activities and play estrogenic activities by different mechanisms. First we used cell proliferation tests to determine the estrogenic activities of these chemicals and to obtain the dose-effect relationship. The results showed the selected environmental estrogens induced cell proliferation. The active dose of E2 was the lowest and estrogen effect of HCB was the highest. The dose-effect relationships of all environmental estrogens accorded with the form of a parabola. E2, BPA, NP could induce estrogen effect and were stronger than others at 48h. DBP, Cd, HCB could induce the estrogen effect and were stronger than others at 72h. DBP, Cd, HCB had cumulative effects and they showed estrogenic activities at different times. Based on the results of single environmental estrogen activity, the activity of multiple environmental estrogens coexisting with E2 was determined. The results showed that E2 decreased the estrogen effect of mixture.
In order to clarify the changes of estrogenic activities for environmental estrogens mixing with E2, the mechanisms were studied. The results showed E2 could weaken estrogen effect of BPA, NP, DBP, Cd and HCB, but synergistic effect occurred when E2 and NP were mixed at 48h. In view of the effect E2 have on the other chemicals, estrogen receptor and MAPK signal channels were studied to determine the affecting mechanisms before and after mix. The results showed E2, NP, DBP, Cd and HCB all could induce cell proliferation by estrogen receptor and MAPK signal channels before and after mix. BPA induced cell proliferation by estrogen receptor, and after mix estrogen receptor and MAPK signal channels were invoked. Different chemicals invoked different downstream transcription factor before and after mix with E2, thus induced cell proliferation.
When the effect of mixture on MCF-7 cells was studied, the effect of mixture on sertoli cells was studied too. Sertoli cells of testis were used to test. Cell proliferation test was used to determine the changes of activities before and after mix of E2 and BPA, NP, DBP, Cd, HCB. Before mix, Cd inhibited the proliferation of sertoli cells, the other chemicals promoted the proliferation of sertoli cells. They all could induce the cell proliferation after mix. The degree of proliferation was inconformity, so the mechanisms should be studied. The results showed E2 could affect the cell proliferation by the progress of cell cycle. BPA invoked the ERK signal channel to induce the cell proliferation, and the mechanism did not change after mix with E2. NP and DBP invoked the JNK signal channel to induce the cell proliferation, and the JNK signal channel still played after mix with E2. Cd inhibited cell proliferation by inhibiting the expression of p-ERK protein, and the inhibiting effect disappeared after mix with E2. HCB invoked the JNK signal channel to induce the cell proliferation, and the mixture of E2 and HCB inhibited cell proliferation by inhibiting the expression of p-ERK protein.
In order to analyze the estrogenic activities of drinking water and ensure the safety of drinking water, the environmental estrogenic activities after mix was studied. The estrogenic activities and mechanisms of raw water, sedimentation water, filtered water, treated water, and tap water were studied. The results showed the treatment processes can reduce estrogenic activity of the raw water. Along with the treatment processes went deeper, estrogenic activity reduced. But the estrogenic activity of tap water was more powerful than treated water, illustrating physical and chemical changes have reacted in the process of transport in drinking water pipe system, and the estrogenic activities of drinking water have changed. To study the male cells toxicities are also important. The results of water sample after all treatment processes inducing the male cells toxicities showed raw water promoted the proliferation of sertoli cells. After various treatments, the water samples showed no effect on male, illustrating that the drinking water treatment processes were effective for male toxicity. Mechanisms of effect of water sample of the all treatment processes on female and male were studied. The results showed raw water, filtered water and finished water could invoke transcription factor C-Myc protein and C-Fos gene by estrogen receptor and ERK signal channel induced cell proliferation. Sedimentation water and tap water not only invoked the estrogen receptor but also invoked the ERK signal channel, invoking the c-Myc gene expression and promoting cell proliferation. The results of male toxicity of drinking water showed raw water inhibited the apoptosis of sertoli cells by invoking the JNK signal channel, inducing the expression of cyclinD1 protein and increasing the number of cells. The other treatment processes reduced the estrogen content in drinking water, so the expression of function protein decreased and no proliferation effects occurred.
本论文选取原水中典型环境雌激素双酚A(BPA)、壬基酚(NP)、邻苯二甲酸二丁酯(DBP)、镉(Cd)和六氯苯(HCB)与雌二醇(E2)混合后进行试验,由于以上五种化合物的来源不同,具有不同的生物活性,同时通过不同的作用机制发挥雌激素活性,因此用于研究与E2混合后的雌激素活性变化具有代表性。首先利用细胞增殖实验对以上环境雌激素进行活性测定,确定量效关系。从结果可知,选取的环境雌激素均能诱导细胞增殖,E2引起雌激素效应的剂量最小,HCB诱导的雌激素效应最强,所有环境雌激素的剂量效应关系都符合抛物线形状。E2、BPA、NP在48h诱导细胞增殖的效应最强,DBP、Cd、HCB在72h诱导细胞增殖的效应最强,DBP、Cd、HCB具有效应累积性,雌激素活性的发挥有时间差别。根据单一环境雌激素检测结果,测定以上环境雌激素与E2混合后的活性变化。结果表明:E2与其他单一及混合环境雌激素联合作用时,主要发挥了弱化作用,减弱了其他单一及混合环境雌激素的雌激素效应。
为了阐明环境雌激素与E2混合后的活性变化,进行了混合活性的机制研究。结果表明:E2与其他环境雌激素联合作用于乳腺癌MCF-7细胞48h,E2对BPA、DBP、Cd、HCB发生弱化作用,但与NP却发生了协同作用。针对E2对其他环境雌激素的这种影响,分别从雌激素受体和丝裂原活化蛋白激酶(MAPK)信号通路的角度进行研究,进而确定联合前后的机制变化。研究发现E2、NP、DBP、Cd和HCB都可以通过雌激素受体和胞外信号调节激酶(ERK)信号途径诱导细胞增殖,而BPA通过受体途径发挥作用。BPA、NP、DBP、Cd和HCB分别与E2混合后,都可以通过雌激素受体和ERK信号途径,激活不同的转录因子,诱导细胞增殖。
同时开展了环境雌激素与E2混合后对大鼠睾丸支持细胞的影响研究。利用细胞增殖试验检测E2与BPA、NP、DBP、Cd、HCB混合后对睾丸支持细胞的影响,以上化合物单独作用时,Cd抑制了细胞的增殖,其他化合物促进了细胞的增殖,联合后均能诱导支持细胞的增殖,但增殖程度不一致,因此对影响机制进行研究,发现E2通过周期调控的机制影响了睾丸支持细胞的增殖;BPA通过激活ERK信号通路诱导增殖,与E2联合后机制不变;NP、DBP通过c-Jun氨基末端激酶(JNK)信号通路发挥的作用,与E2联合后这种JNK通路依然发挥作用;Cd通过抑制p-ERK蛋白发挥抑制作用,与E2联合后,抑制作用消失;HCB是通过激活了JNK信号通路诱导细胞增殖,与E2联合组是通过抑制p-ERK而发挥抑制作用。
研究环境雌激素与E2混合后的活性,最终是要对饮用水的雌激素活性进行分析,保障饮用水的安全。对原水、沉后水、滤后水、出厂水及管网水的雌激素活性及其作用机制进行研究。结果表明各处理工艺能够有效的降低原水的雌激素活性,随着处理工艺的深入,活性降低。出厂水雌激素活性消失,但管网水较出厂水雌激素活性稍有增高,表明在管网运输过程中发生了物理化学变化,改变了水中环境雌激素的性质。饮用水各处理工艺出水对睾丸支持细胞的影响同样是研究的重点,研究结果表明,原水能够促进睾丸支持细胞增殖,随着处理工艺的深入,其他单元出水对睾丸支持细胞几乎没有影响,说明水处理工艺能够有效的降低环境雌激素的生物活性。在此基础上,对饮用水各处理工艺出水内分泌干扰的机制进行研究,结果表明:对乳腺癌MCF-7细胞的影响机制为,原水、滤后水和出厂水通过雌激素受体途径和p-ERK信号通路激活核内转录因子c-Myc蛋白和c-Fos基因发挥增殖作用,而沉后水、管网水可以通过雌激素受体通路和ERK信号通路诱导c-Myc蛋白表达进而促进细胞增殖。滤后水还可以通过c-Jun基因的激活诱导增殖。对睾丸支持细胞影响的机制为,原水通过激活p-JNK信号通路,诱导cyclinD1蛋白表达,抑制了细胞的凋亡进而增加了细胞的数量,而其他各处理工艺出水中环境雌激素含量减少,因此对蛋白诱导的能力降低,没有诱导支持细胞增殖。
The serious source water pollution in China, especially the pollution by environmental estrogens, has caused widespread concerns. The environmental estrogens are of great health hazards and are hard to be removed. Environmental estrogens mainly exist as mixtures and function together with E2 in the environment and in vivo. So it is of important practical significance to study the activity when multiple environmental estrogens coexist with E2.
Six typical estrogens in water source were selected, namely E2, BPA, NP, DBP, Cd, and HCB. These estrogens are of different sources, have different biological activities and play estrogenic activities by different mechanisms. First we used cell proliferation tests to determine the estrogenic activities of these chemicals and to obtain the dose-effect relationship. The results showed the selected environmental estrogens induced cell proliferation. The active dose of E2 was the lowest and estrogen effect of HCB was the highest. The dose-effect relationships of all environmental estrogens accorded with the form of a parabola. E2, BPA, NP could induce estrogen effect and were stronger than others at 48h. DBP, Cd, HCB could induce the estrogen effect and were stronger than others at 72h. DBP, Cd, HCB had cumulative effects and they showed estrogenic activities at different times. Based on the results of single environmental estrogen activity, the activity of multiple environmental estrogens coexisting with E2 was determined. The results showed that E2 decreased the estrogen effect of mixture.
In order to clarify the changes of estrogenic activities for environmental estrogens mixing with E2, the mechanisms were studied. The results showed E2 could weaken estrogen effect of BPA, NP, DBP, Cd and HCB, but synergistic effect occurred when E2 and NP were mixed at 48h. In view of the effect E2 have on the other chemicals, estrogen receptor and MAPK signal channels were studied to determine the affecting mechanisms before and after mix. The results showed E2, NP, DBP, Cd and HCB all could induce cell proliferation by estrogen receptor and MAPK signal channels before and after mix. BPA induced cell proliferation by estrogen receptor, and after mix estrogen receptor and MAPK signal channels were invoked. Different chemicals invoked different downstream transcription factor before and after mix with E2, thus induced cell proliferation.
When the effect of mixture on MCF-7 cells was studied, the effect of mixture on sertoli cells was studied too. Sertoli cells of testis were used to test. Cell proliferation test was used to determine the changes of activities before and after mix of E2 and BPA, NP, DBP, Cd, HCB. Before mix, Cd inhibited the proliferation of sertoli cells, the other chemicals promoted the proliferation of sertoli cells. They all could induce the cell proliferation after mix. The degree of proliferation was inconformity, so the mechanisms should be studied. The results showed E2 could affect the cell proliferation by the progress of cell cycle. BPA invoked the ERK signal channel to induce the cell proliferation, and the mechanism did not change after mix with E2. NP and DBP invoked the JNK signal channel to induce the cell proliferation, and the JNK signal channel still played after mix with E2. Cd inhibited cell proliferation by inhibiting the expression of p-ERK protein, and the inhibiting effect disappeared after mix with E2. HCB invoked the JNK signal channel to induce the cell proliferation, and the mixture of E2 and HCB inhibited cell proliferation by inhibiting the expression of p-ERK protein.
In order to analyze the estrogenic activities of drinking water and ensure the safety of drinking water, the environmental estrogenic activities after mix was studied. The estrogenic activities and mechanisms of raw water, sedimentation water, filtered water, treated water, and tap water were studied. The results showed the treatment processes can reduce estrogenic activity of the raw water. Along with the treatment processes went deeper, estrogenic activity reduced. But the estrogenic activity of tap water was more powerful than treated water, illustrating physical and chemical changes have reacted in the process of transport in drinking water pipe system, and the estrogenic activities of drinking water have changed. To study the male cells toxicities are also important. The results of water sample after all treatment processes inducing the male cells toxicities showed raw water promoted the proliferation of sertoli cells. After various treatments, the water samples showed no effect on male, illustrating that the drinking water treatment processes were effective for male toxicity. Mechanisms of effect of water sample of the all treatment processes on female and male were studied. The results showed raw water, filtered water and finished water could invoke transcription factor C-Myc protein and C-Fos gene by estrogen receptor and ERK signal channel induced cell proliferation. Sedimentation water and tap water not only invoked the estrogen receptor but also invoked the ERK signal channel, invoking the c-Myc gene expression and promoting cell proliferation. The results of male toxicity of drinking water showed raw water inhibited the apoptosis of sertoli cells by invoking the JNK signal channel, inducing the expression of cyclinD1 protein and increasing the number of cells. The other treatment processes reduced the estrogen content in drinking water, so the expression of function protein decreased and no proliferation effects occurred.
引文
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