铜抑制了升高温度诱导的紫红圆海胆胚胎应激蛋白合成。

B M Sanders, L S Martin
{"title":"铜抑制了升高温度诱导的紫红圆海胆胚胎应激蛋白合成。","authors":"B M Sanders,&nbsp;L S Martin","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>A major component of the cellular stress response entails the induced synthesis of a suite of stress proteins under environmentally adverse conditions that functions to protect organisms from environmentally induced damage. Here, we examined induction of the stress response in the embryos of the sea urchin Strongylocentrus purpuratus under a combination of environmentally realistic conditions. First, we examined the response elicited over a range of free cupric ion activities, (Cu2+), using a metal buffer system to control trace metal speciation. We observed no pronounced differences in translational patterns in embryos exposed to free cupric ion activities, (Cu2+), of 10(-13)-10(-9) M by metabolic labeling, 1-dimensional electrophoresis and autoradiography. Further separation by 2-dimensional electrophoresis, however, revealed electrophoretically discernable variants of several groups of proteins at the higher Cu concentrations and the synthesis of a 60 kDa protein at (Cu2+) of 10(-9) M. In addition, there were differences in the stress response induced by heat-shock treatment in embryos cultured in seawater with different Cu concentrations; radiolabel was incorporated into a greater number of cellular proteins in embryos at lower (Cu2+) and the induced synthesis of stress proteins was greater. These data suggest that elevations in (Cu2+) impair the ability of the embryos to mount the stress response upon exposure to elevated temperatures and that Cu may alter critical developmental pathways by inhibiting the synthesis of regulatory proteins. Such effects on gene expression can result in manifestations that have been widely attributed to Cu toxicity, including developmental abnormalities and increased sensitivity to environmental extremes. We suggest that the particular sensitivity of embryonic systems upon exposure to multiple stressors may be a consequence of these mechanisms.</p>","PeriodicalId":79328,"journal":{"name":"Comparative biochemistry and physiology. Part C, Pharmacology, toxicology & endocrinology","volume":"109 3","pages":"295-307"},"PeriodicalIF":0.0000,"publicationDate":"1994-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Copper inhibits the induction of stress protein synthesis by elevated temperatures in embryos of the sea urchin Strongylocentrus purpuratus.\",\"authors\":\"B M Sanders,&nbsp;L S Martin\",\"doi\":\"\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>A major component of the cellular stress response entails the induced synthesis of a suite of stress proteins under environmentally adverse conditions that functions to protect organisms from environmentally induced damage. Here, we examined induction of the stress response in the embryos of the sea urchin Strongylocentrus purpuratus under a combination of environmentally realistic conditions. First, we examined the response elicited over a range of free cupric ion activities, (Cu2+), using a metal buffer system to control trace metal speciation. We observed no pronounced differences in translational patterns in embryos exposed to free cupric ion activities, (Cu2+), of 10(-13)-10(-9) M by metabolic labeling, 1-dimensional electrophoresis and autoradiography. Further separation by 2-dimensional electrophoresis, however, revealed electrophoretically discernable variants of several groups of proteins at the higher Cu concentrations and the synthesis of a 60 kDa protein at (Cu2+) of 10(-9) M. In addition, there were differences in the stress response induced by heat-shock treatment in embryos cultured in seawater with different Cu concentrations; radiolabel was incorporated into a greater number of cellular proteins in embryos at lower (Cu2+) and the induced synthesis of stress proteins was greater. These data suggest that elevations in (Cu2+) impair the ability of the embryos to mount the stress response upon exposure to elevated temperatures and that Cu may alter critical developmental pathways by inhibiting the synthesis of regulatory proteins. Such effects on gene expression can result in manifestations that have been widely attributed to Cu toxicity, including developmental abnormalities and increased sensitivity to environmental extremes. We suggest that the particular sensitivity of embryonic systems upon exposure to multiple stressors may be a consequence of these mechanisms.</p>\",\"PeriodicalId\":79328,\"journal\":{\"name\":\"Comparative biochemistry and physiology. Part C, Pharmacology, toxicology & endocrinology\",\"volume\":\"109 3\",\"pages\":\"295-307\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"1994-11-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Comparative biochemistry and physiology. Part C, Pharmacology, toxicology & endocrinology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Comparative biochemistry and physiology. Part C, Pharmacology, toxicology & endocrinology","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

摘要

细胞应激反应的一个主要组成部分需要在环境不利条件下诱导合成一套应激蛋白,其功能是保护生物体免受环境诱导的损害。在此,我们研究了在环境现实条件下海胆胚胎应激反应的诱导。首先,我们研究了在一系列自由铜离子活性(Cu2+)中引发的反应,使用金属缓冲系统来控制痕量金属形态。通过代谢标记、1维电泳和放射自显影,我们观察到10(-13)-10(-9)M游离铜离子活性(Cu2+)暴露的胚胎的翻译模式没有明显差异。然而,通过二维电泳进一步分离发现,在较高Cu浓度下,有几组蛋白在电泳上可识别变异,在(Cu2+)为10(-9)m时,合成了一个60 kDa的蛋白。此外,不同Cu浓度海水中培养的胚胎在热休克诱导的应激反应中存在差异;低Cu2+条件下,胚胎细胞蛋白中放射性标记的掺入量较大,诱导应激蛋白的合成量较大。这些数据表明,(Cu2+)的升高会损害胚胎在高温下产生应激反应的能力,并且Cu可能通过抑制调节蛋白的合成来改变关键的发育途径。这种对基因表达的影响可能导致广泛归因于铜毒性的表现,包括发育异常和对极端环境的敏感性增加。我们认为,胚胎系统在暴露于多种应激源时的特殊敏感性可能是这些机制的结果。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Copper inhibits the induction of stress protein synthesis by elevated temperatures in embryos of the sea urchin Strongylocentrus purpuratus.

A major component of the cellular stress response entails the induced synthesis of a suite of stress proteins under environmentally adverse conditions that functions to protect organisms from environmentally induced damage. Here, we examined induction of the stress response in the embryos of the sea urchin Strongylocentrus purpuratus under a combination of environmentally realistic conditions. First, we examined the response elicited over a range of free cupric ion activities, (Cu2+), using a metal buffer system to control trace metal speciation. We observed no pronounced differences in translational patterns in embryos exposed to free cupric ion activities, (Cu2+), of 10(-13)-10(-9) M by metabolic labeling, 1-dimensional electrophoresis and autoradiography. Further separation by 2-dimensional electrophoresis, however, revealed electrophoretically discernable variants of several groups of proteins at the higher Cu concentrations and the synthesis of a 60 kDa protein at (Cu2+) of 10(-9) M. In addition, there were differences in the stress response induced by heat-shock treatment in embryos cultured in seawater with different Cu concentrations; radiolabel was incorporated into a greater number of cellular proteins in embryos at lower (Cu2+) and the induced synthesis of stress proteins was greater. These data suggest that elevations in (Cu2+) impair the ability of the embryos to mount the stress response upon exposure to elevated temperatures and that Cu may alter critical developmental pathways by inhibiting the synthesis of regulatory proteins. Such effects on gene expression can result in manifestations that have been widely attributed to Cu toxicity, including developmental abnormalities and increased sensitivity to environmental extremes. We suggest that the particular sensitivity of embryonic systems upon exposure to multiple stressors may be a consequence of these mechanisms.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
自引率
0.00%
发文量
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信