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首页> 外文期刊>ACS applied materials & interfaces >Tumor-Specific Expansion of Oxidative Stress by Glutathione Depletion and Use of a Fenton Nanoagent for Enhanced Chemodynamic Therapy
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Tumor-Specific Expansion of Oxidative Stress by Glutathione Depletion and Use of a Fenton Nanoagent for Enhanced Chemodynamic Therapy

机译：通过谷胱甘肽耗尽和使用Fenton纳米代购的肿瘤特异性膨胀氧化应激以增强化学正动疗法

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摘要

Amplifying intracellular oxidative stress effectively destroys cancer cells. In addition, iron-mediated Fenton reaction converts endogenous H2O2 to produce hypertoxic hydroxyl radical ((OH)-O-center dot), resulting in irreversible oxidative damage to combat tumor cells. This method is known as chemodynamic therapy (CDT). Overexpressed glutathione (GSH) in tumor cells efficiently scavenges (OH)-O-center dot, significantly reducing the curative effects of CDT. To overcome this challenge and enhance intracellular oxidative stress, iron oxide nanocarriers loaded with beta-lapachone (Lapa) drugs (Fe3O4-HSA@Lapa) were constructed and had both Fenton-like agents and GSH depletion properties to amplify intracellular oxidative stress. Release of Lapa selectively increases tumor site-specific generation of H2O2 via NAD(P)H: quinone oxidoreductase 1 (NQO1) catalysis. Subsequently, the iron ions released from the ionization of Fe3O4 in the acidic environment selectively convert H2O2 into highly toxic (OH)-O-center dot by Fenton reaction, dramatically improving CDT with minimal systemic toxicity due to low NQO1 expression in normal tissues. Meanwhile, released Lapa consumes GSH in the tumor, amplifying oxidative stress and enhancing the efficacy of CDT. Designed Fe3O4-HSA@Lapa nanoparticles (NPs) exhibit perfect targeting capability, prolonged blood circulation, and increased tumor accumulation. Furthermore, Fe3O4-HSA@Lapa NPs effectively enhance the inhibition of tumor growth and reduce the side effects of anticancer drugs. This work establishes a remarkably enhanced tumor-selective CDT against NQO1-overexpressing tumors by significantly inducing intratumoral oxidative stress with minimal side effects.
机译：扩增细胞内氧化应激有效地破坏癌细胞。此外，铁介导的芬顿反应转化内源性H 2 O 2以产生高氧态羟基自由基（（OH）-O中心点），导致对抗肿瘤细胞的不可逆氧化损伤。该方法称为化学动力学治疗（CDT）。肿瘤细胞的过度表达谷胱甘肽（GSH）有效地清除（OH）-O-中心点，显着降低了CDT的疗效。为了克服这种挑战并增强细胞内氧化应激，构建了β-乙酰酮（LAPA）药物（Fe3O4-HSA-HAPA）的氧化铁纳米载体（Fe3O4-Hsa -,6），并具有Fenton样剂和GSH耗尽性能以扩增细胞内氧化应激。释放LAPA通过NAD（P）H：醌氧化还原酶1（NQO1）催化增加肿瘤位点特异性的H 2 O 2。随后，在酸性环境中从Fe3O4的电离中释放的铁离子选择性地将H 2 O 2转化为高毒性（OH）-o中心点，通过芬顿反应显着改善CDT，由于正常组织中的低NQO1表达，由于低NQO1表达而具有最小的全身毒性。同时，释放的拉帕在肿瘤中消耗GSH，扩增氧化应激并提高CDT的功效。设计Fe3O4-HSA @ LAPA纳米颗粒（NPS）表现出完善的靶向能力，延长血液循环和增加的肿瘤积累。此外，Fe3O4-HSA @ Lapa NPS有效增强肿瘤生长的抑制，降低抗癌药物的副作用。通过显着诱导腹部氧化应激，副作用最小氧化应激，这项工作通过显着诱导腹腔氧化胁迫来建立显着增强的肿瘤选择性CDT。

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  • 来源
    《ACS applied materials & interfaces》 |2019年第34期|共15页
  • 作者

    Chen Qiufang; Zhou Jun; Chen Zhe; Luo Qing; Xu Jian; Song Guanbin;

  • 作者单位

    Chongqing Univ Coll Bioengn Key Lab Biorheol Sci &

    Technol Minist Educ Chongqing 400030 Peoples R China;

    Chongqing Univ Sch Life Sci Chongqing 400030 Peoples R China;

    Chongqing Univ Coll Bioengn Key Lab Biorheol Sci &

    Technol Minist Educ Chongqing 400030 Peoples R China;

    Chongqing Univ Coll Bioengn Key Lab Biorheol Sci &

    Technol Minist Educ Chongqing 400030 Peoples R China;

    Chongqing Univ Canc Hosp Chongqing Key Lab Translat Res Canc Metastasis &

    Chongqing 400030 Peoples R China;

    Chongqing Univ Coll Bioengn Key Lab Biorheol Sci &

    Technol Minist Educ Chongqing 400030 Peoples R China;

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  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 化学工业;
  • 关键词

    destruction of redox homeostasis; beta-lapachone; iron oxide; Fenton's reaction; GSH depletion;

    机译：德罗德稳态的破坏;β-乙酰酮;氧化铁;芬顿的反应;GSH消耗;

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