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首页> 外文期刊>Environmental toxicology and chemistry >PERFLUOROOCTANE SULFONIC ACID EXPOSURE INCREASES CADMIUM TOXICITY IN EARLY LIFE STAGE OF ZEBRAFISH, DANIO RERIO
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PERFLUOROOCTANE SULFONIC ACID EXPOSURE INCREASES CADMIUM TOXICITY IN EARLY LIFE STAGE OF ZEBRAFISH, DANIO RERIO

机译:全氟辛烷磺酸暴露会增加斑马鱼,丹尼埃里奥(DANIO RERIO)早期生命阶段的镉毒性

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摘要

Exposure to perfluorooctane sulfonic acid (PFOS) is known to induce thyroid-related adverse effects in aquatic organisms. Because an antioxidant defense mechanism is one of the key functions of the thyroid gland, we examined whether preexposure to PFOS could disrupt thyroid function and enhance cadmium (Cd)-induced oxidative stress in fish. Zebrafish embryos were exposed to control or 0.5 mg/L PFOS for 7 d after fertilization and subsequently exposed to 0.038 mg/L of Cd~(2+) or a mixture of the PFOS and Cd for an additional 3 d until 10 d postfertilization (dpf). Survival rates, body length, messenger RNA (mRNA) expressions related to thyroid function and oxidative stress, the levels of thyroid hormones, and malondialdehyde and antioxidant enzyme activities were measured. Significant down-regulation of mRNAs related to thyroid function (thyroid hormone receptor-alpha [THRa], thyroid hormone receptor-beta [THRfi], hematopoietically expressed homeobox [hhex], and paired box gene 8 [pax8]) and decrease of throxine (T4) levels were observed in the PFOS preexposure group, suggesting that PFOS preexposure would influence the performance of thyroid gland in the later stages of life. Certain genes relative to oxidative stress, such as superoxide dismutase 1 (sodl) and heat shock protein 70 (hsp70), in the PFOS preexposure group were significantly up-regulated when the larvae were subsequently exposed to Cd or to the mixture of PFOS and Cd. Glutathione 5-transferase activity and malondialdehyde levels of the PFOS-preexposed group were increased significantly by Cd exposure. Significant decrease of the survival rates and body length of fish were observed at 10 dpf among the larvae that were previously exposed to PFOS. These results suggest that preexposure to PFOS could affect antioxidant defense mechanisms and potentially increase the toxicity of Cd on mRNA expression and enzyme activity level responses, as well as on survival or growth of individuals.
机译:已知全氟辛烷磺酸(PFOS)的接触会在水生生物中诱发甲状腺相关的不良影响。因为抗氧化剂防御机制是甲状腺的关键功能之一,所以我们检查了预接触全氟辛烷磺酸是否会破坏甲状腺功能并增强镉(Cd)诱导的鱼的氧化应激。受精后将斑马鱼胚胎暴露于对照或0.5 mg / L PFOS下7 d,随后再暴露于0.038 mg / L Cd〜(2+)或PFOS和Cd的混合物中3 d,直到受精后10 d( dpf)。测量存活率,体长,与甲状腺功能和氧化应激有关的信使RNA(mRNA)表达,甲状腺激素水平以及丙二醛和抗氧化酶活性。与甲状腺功能(甲状腺激素受体-α[THRa],甲状腺激素受体-β[THRfi],造血表达的同源异型框[hhex]和配对框基因8 [pax8])相关的mRNA显着下调,甲状腺素降低(在全氟辛烷磺酸预暴露组中观察到T4)水平,这表明全氟辛烷磺酸预暴露会影响生命后期的甲状腺功能。当幼虫随后暴露于Cd或PFOS和Cd的混合物中时,PFOS预暴露组中与氧化应激有关的某些基因,例如超氧化物歧化酶1(sodl)和热休克蛋白70(hsp70),被显着上调。 。暴露于Cd可使PFOS暴露组的谷胱甘肽5-转移酶活性和丙二醛水平显着提高。在先前接触全氟辛烷磺酸的幼虫中,在10 dpf处观察到鱼的存活率和体长显着下降。这些结果表明,预接触全氟辛烷磺酸可能会影响抗氧化剂的防御机制,并可能增加镉对mRNA表达和酶活性水平反应以及对个体存活或生长的毒性。

著录项

  • 来源
    《Environmental toxicology and chemistry》 |2011年第4期|p.870-877|共8页
  • 作者单位

    School of Public Health, Seoul National University, Seoul, Korea;

    School of Public Health, Seoul National University, Seoul, Korea;

    School of Public Health, Seoul National University, Seoul, Korea;

    School of Public Health, Seoul National University, Seoul, Korea;

    School of Public Health, Seoul National University, Seoul, Korea;

    School of Public Health, Seoul National University, Seoul, Korea;

    Eulji University, Seongnam, Gyeonggi, Korea;

    School of Public Health, Seoul National University, Seoul, Korea;

  • 收录信息 美国《科学引文索引》(SCI);美国《工程索引》(EI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

    mixture toxicity; oxidative stress; thyroid hormone; larvae; cadmium toxicity;

    机译:混合物毒性;氧化应激甲状腺激素幼虫镉毒性;

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