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首页> 外文期刊>Environmental Science & Technology >Protein Fe-S Centers as a Molecular Target of Toxicity of a Complex Transition Metal Oxide Nanomaterial with Downstream Impacts on Metabolism and Growth
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Protein Fe-S Centers as a Molecular Target of Toxicity of a Complex Transition Metal Oxide Nanomaterial with Downstream Impacts on Metabolism and Growth

机译：蛋白质Fe-S中心作为复杂过渡金属氧化物纳米材料的毒性的分子靶标，下游影响对代谢和生长

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摘要

Oxidative stress is frequently identified as a mechanism of toxicity of nanomaterials. However, rarely have the specific underlying molecular targets responsible for these impacts been identified. We previously demonstrated significant negative impacts of transition metal oxide (TMO) lithium-ion battery cathode nanomaterial, lithium cobalt oxide (LCO), on the growth, development, hemoglobin, and heme synthesis gene expression in the larvae of a model sediment invertebrate Chironomus riparius. Here, we propose that alteration of the Fe-S protein function by LCO is a molecular initiating event leading to these changes. A 10 mg/L LCO exposure causes significant oxidation of the aconitase 4Fe-4S center after 7 d as determined from the electron paramagnetic resonance spectroscopy measurements of intact larvae and a significant reduction in the aconitase activity of larval protein after 48 h (p < 0.05). Next-generation RNA sequencing identified significant changes in the expression of genes involved in 4Fe-4S center binding, Fe-S center synthesis, iron ion binding, and metabolism for 10 mg/L LCO at 48 h (FDR-adjusted, p < 0.1). We propose an adverse outcome pathway, where the oxidation of metabolic and regulatory Fe-S centers of proteins by LCO disrupts metabolic homeostasis, which negatively impacts the growth and development, a mechanism that may apply for these conserved proteins across species and for other TMO nanomaterials.
机译：氧化应激经常被鉴定为纳米材料的毒性机制。然而，很少鉴定负责这些影响的特定潜在的分子靶标。我们以前表现出过渡金属氧化物（TMO）锂离子电池阴极纳米材料，锂钴氧化物（LCO）的显着负面影响，对模型沉积物无脊椎动物的幼虫在幼虫中的生长，发育，血红蛋白和血红素合成基因表达中。在这里，我们提出LCO改变FE-S蛋白功能的函数是导致这些变化的分子启动事件。从完整幼虫的电子顺磁共振光谱测量和幼虫蛋白的Aconitase活性的显着降低，10mg / L LCO暴露在7d之后导致遮阳酶4FE-4S中心的显着氧化在7d中，从而在48小时后的幼虫蛋白的穴位酶活性显着降低（P <0.05 ）。下一代RNA测序鉴定了4FE-4S中心结合，Fe-Sent合成，铁离子结合和10mg / L LCO所涉及的基因表达的显着变化在48小时（FDR调节，P <0.1 ）。我们提出了一种不良的结果途径，其中LCO蛋白质的代谢和调节费用氧化扰动了代谢稳态，这会对生长和发展产生负面影响，这是一种可以跨越物种和其他TMO纳米材料对这些保守蛋白质的机制。

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  • 来源
    《Environmental Science & Technology》 |2020年第23期|15257-15266|共10页
  • 作者

    Nicholas J. Niemuth; Yonqian Zhang; Aurash A. Mohaimani; Angela Schmoldt; Elizabeth D. Laudadio; Robert J. Hamers; Rebecca D. Klaper;

  • 作者单位

    School of Freshwater Sciences University of Wisconsin-Milwaukee Milwaukee Wisconsin 53204 United States;

    Department of Chemistry University of Wisconsin-Madison Madison Wisconsin 53706 United States;

    School of Freshwater Sciences University of Wisconsin-Milwaukee Milwaukee Wisconsin 53204 United States;

    School of Freshwater Sciences University of Wisconsin-Milwaukee Milwaukee Wisconsin 53204 United States;

    Department of Chemistry University of Wisconsin-Madison Madison Wisconsin 53706 United States;

    Department of Chemistry University of Wisconsin-Madison Madison Wisconsin 53706 United States;

    School of Freshwater Sciences University of Wisconsin-Milwaukee Milwaukee Wisconsin 53204 United States;

  • 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);
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