...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Toxicology Letters: An International Journal Providing a Forum for Original and Pertinent Contributions in Toxicology Research >Potentiation of arsenic-induced cytotoxicity by sulfur amino acid deprivation (SAAD) through activation of ERK1/2, p38 kinase and JNK1: the distinct role of JNK1 in SAAD-potentiated mercury toxicity.
【24h】

Potentiation of arsenic-induced cytotoxicity by sulfur amino acid deprivation (SAAD) through activation of ERK1/2, p38 kinase and JNK1: the distinct role of JNK1 in SAAD-potentiated mercury toxicity.

机译：通过激活ERK1 / 2，p38激酶和JNK1增强硫氨基酸剥夺（SAAD）诱导的砷引起的细胞毒性：JNK1在SAAD增强的汞毒性中的独特作用。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Sulfur amino acid deficiency occurs in certain pathophysiological situations (e.g. protein-calorie malnutrition). Previous studies revealed that sulfur amino acid deprivation (SAAD) activated MAP kinases and potentiated cadmium-induced cytotoxicity by activation of ERK1/2 in conjunction with p38 kinase or JNK. The present study was designed to determine susceptibility of cells to a variety of heavy metals in combination with SAAD. Viability was assessed in H4IIE cells treated with sodium arsenite, mercuric chloride, sodium selenite, lead acetate, chromium trioxide or manganese chloride. SAAD potentiated the cytotoxicity of H4IIE cells by arsenic or mercury (i.e. EC50, 19 and 5 microM in SAAD vs. 401 and 42 microM in control medium, respectively). TUNEL assays revealed that the potentiated arsenic or mercury toxicity involved apoptotic cell death. Lead or selenite moderately elicited cell death, which was not enhanced by SAAD. Chromium or manganese caused no significant cytotoxicity. Treatment of cells with U0126 [1,4-diamino-2,3-dicyano-1,4-bis(2-aminophenylthio)butadiene] an ERK1/2 inhibitor or SB203580 [4-(4-fluorophenyl)-2-(4-methylsulfinylphenyl)-5-(4-pyridyl)1H-imidazole] a p38 kinase inhibitor effectively prevented SAAD-potentiated arsenic toxicity. The potentiated arsenic toxicity was also inhibited in cells stably expressing a dominant negative mutant of c-Jun N-terminal kinase 1 [JNK1(-)]. The inhibitors of extracellular signal-regulated kinase 1/2 (ERK1/2) and p38 kinase failed to prevent mercury-induced toxicity enhanced by SAAD. JNK1(-) cells were minimally susceptible to mercury in SAAD medium. These results demonstrated that SAAD potentiated cytotoxicity induced by arsenic or mercury and that activation of ERK1/2, p38 kinase and JNK1 was responsible for the potentiated arsenic toxicity, whereas the mercury toxicity enhanced by SAAD was mediated with the activity of JNK1.
机译：某些病理生理情况下会发生硫氨基酸缺乏症（例如蛋白质热量不足营养不良）。先前的研究表明，硫氨基酸剥夺（SAAD）通过与p38激酶或JNK结合激活ERK1 / 2来激活MAP激酶并增强镉诱导的细胞毒性。本研究旨在与SAAD一起确定细胞对多种重金属的敏感性。在用亚砷酸钠，氯化汞，亚硒酸钠，乙酸铅，三氧化铬或氯化锰处理的H4IIE细胞中评估了活力。 SAAD通过砷或汞来增强H4IIE细胞的细胞毒性（即SAAD中的EC50、19和5 microM，对照培养基中的EC50、401和42 microM）。 TUNEL分析显示，增强的砷或汞毒性涉及凋亡细胞死亡。铅或亚硒酸盐可中等程度地引起细胞死亡，而SAAD并不能增强这种死亡。铬或锰不会引起明显的细胞毒性。用ERK1 / 2抑制剂或SB203580 [4-（4-氟苯基）-2-（4）用U0126 [1,4-二氨基-2,3-二氰基-1,4-双（2-氨基苯硫基）丁二烯]处理细胞-p38激酶抑制剂可有效预防SAAD增强的砷中毒。-甲基亚磺酰基苯基）-5-（4-吡啶基）1H-咪唑]在稳定表达c-Jun N端激酶1 [JNK1（-）]的显性负突变体的细胞中，也增强了砷的毒性。细胞外信号调节激酶1/2（ERK1 / 2）和p38激酶的抑制剂未能阻止SAAD增强汞诱导的毒性。在SAAD培养基中，JNK1（-）细胞对汞的敏感性最低。这些结果表明，SAAD增强了砷或汞诱导的细胞毒性，而ERK1 / 2，p38激酶和JNK1的激活是增强砷毒性的原因，而SAAD增强的汞毒性是由JNK1的活性介导的。

著录项

相似文献

  • 外文文献
  • 中文文献
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号