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ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY · 2025 · IF 6.1

Benzothiazole kills Meloidogyne incognita quickly by inhibiting GST to trigger ROS bursting

Qiyi Zhu,Xiaofeng Zhu,Ning Yang,Yuxi Duan,Yuanyuan Wang,Xiaoyu Liu,Di Zhao,Haiyan Fan,Lijie Chen

Root-knot nematodes ( Meloidogyne incognita ) present a significant threat to global agriculture, and the development of multi-drug resistance in these nematodes exacerbates this problem. Benzothiazole, a heterocyclic compound has been reported as a potential nematicide, however, its mode of action is not fully understood. This study aims to elucidate the nematicidal mechanism of benzothiazole against M. incognita . In the toxicity assays, benzothiazole exhibited rapid and effective nematocidal activity, significantly compromising egg masses and inhibiting egg hatching while killing newly hatched second-stage juveniles (J2s) of M. incognita . Microscopic observations revealed that after 48 h of incubation, a marked reduction in protein and carbohydrate levels within the J2s was observed. Notably, benzothiazole at a concentration of 14 mmol/L significantly inhibits glutathione S-transferase (GST) enzyme activity, leading to the accumulation of reactive oxygen species (ROS), ultimately resulting in rapid nematode death. Molecular docking and dynamics simulations demonstrated that benzothiazole forms a stable complex with GST, thereby disrupting its antioxidant function. Furthermore, in pot experiments, benzothiazole effectively reduced the gall formations of M. incognita on tomato roots. Overall, this novel inhibitory mechanism of glutathione S-transferase (GST) differs from that of the neurotoxicant abamectin, which targets glutamate-gated chloride channels (GluCl). This mechanism holds significant promise for the development of environmentally friendly nematicides. It offers a potential solution to the growing problem of multidrug resistance in root-knot nematodes and could help mitigate the substantial economic losses caused by these pests in global agriculture.

CAS / MDL: 95-16-9
研究领域: 农业科学 · 害虫防治 · 生物化学 · 线虫学 · 植物病理学
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Bioactive Materials · 2025 · IF 20.3

Sonotheranostic nanosideromycin eradicates bacterial biofilm infections via ultrasound-detonated ROS generation and ferroptosis-like death

Xin Pang,Chang Zhang,Qicai Xiao,Yi Cheng,Qixuan Dai,Hu Chen,Sijia Tan,Gang Liu,Yun Zeng

Biofilm formation poses a severe challenge to antibacterial stewardship. While siderophore-antibiotic conjugates (termed as sideromycins) offer a promising solution, their efficacy is inherently limited by antibiotic resistance. To transcend this barrier, we pioneer a transformative siderophore-sonosensitizer conjugate through covalent linkage of a catechol siderophore to purpurin 18 (a sonosensitizer). This novel conjugate further self-assembles with iron(III) ions, forming the first-reported carrier-free nanosideromycin—an all-in-on iron-siderophore-sonosensitizer nanoplatform. This design enables ultrasound-denotated reactive oxygen species (ROS) generation and ferroptosis-like amplication. Capitalizing on bacteria-specific siderophore uptake and pH-responsive assembly/disassembly, the nanosideromycin enables precision delivery and active internalization of sonosensitizers into bacteria. This strategy permits real-time localization of infections via concurrent fluorescence/photoacoustic and magnetic resonance imaging. Upon ultrasound irradiation, dual antimicrobial mechanisms of sonosensitizer-mediated sonodynamic therapy and siderophore/iron-augmented sono-Fenton catalysis are stimuonously unleashed, synergistically tirggering an explosive ROS burst and potent ferroptosis-like bacterial death. As a result, mice with multidrug-resistant biofilm-induced pyomyositis were completely cured. Collectively, this first-in-class theranostic nanosideromycin integrates highly-targeted imaging diagnostics, cost-effective yet ultra-efficient ROS generation, and ferroptosis-like bacterial killing, establishing a paradigm-shifting strategy for biofilm therapy with spatiotemporal controllability.

研究领域: 微生物学 · 纳米医学 · 感染性疾病 · 分子影像学 · 抗菌治疗 · 自由基生物学 · 药物递送系统
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CARBOHYDRATE POLYMERS · 2024 · IF 10.7

A chemo/chemodynamic nanoparticle based on hyaluronic acid induces ferroptosis and apoptosis for triple-negative breast cancer therapy

Ning Wang,Qiyu Zhang,Zhuoya Wang,Yichao Liu,Sen Yang,Xuerong Zhao,Jinyong Peng

Triple-negative breast cancer (TNBC) poses a serious threat to women's life and health due to its high malignancy, strong invasiveness, and propensity for early recurrence and metastasis. Therefore, there is an urgent need to develop a highly effective and low-toxic TNBC treatment scheme to enhance the anti-cancer efficacy and prolong the survival of patients. In this work, we designed and synthesized a chemodynamic therapy (CDT) agent (HA-Fc-Mal). The chemo/chemodynamic (CT/CDT) nanoparticle (HCM@DOX) based on hyaluronic acid induces ferroptosis and apoptotic for TNBC therapy was constructed via self-assembled of HA-Fc-Mal and doxorubicin (DOX). HCM@DOX orderly realized the TNBC targeting, controlled DOX release, GSH depletion and induce ROS erupt. In vivo and in vitro experiments confirmed that HCM@DOX inhibited the growth of 4 T1 tumors through ferroptosis and apoptosis, and the tumor inhibition rate was as high as 81.87 %. In addition, HCM@DOX significantly inhibited lung metastasis and exhibited excellent biosafety. Overall, our findings offer a new strategy for TNBC therapy using a CT/CDT nanoparticle that induces ferroptosis and apoptosis.

研究领域: 肿瘤学 · 纳米技术 · 药学 · 生物医学工程
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Nature Communications · 2025 ·Vol. 16 ·期 1 ·1-23 · IF 15.7

Engineering nanozyme immunomodulator with magnetic targeting effect for cascade-enzyodynamic and ultrasound-reinforced metallo-immunotherapy in prostate carcinoma

Wang Yandong,Li Haodong,Lin Junyang,Li Yutang,Zhang Keqin,Li Hui,Fu Qiang,Jiang Yanyan

Conventional immunotherapy exhibits low response rates due to the immunosuppressive tumor microenvironment (TME). To overcome this limitation, this study introduces ZFPG nanoparticles (ZFPG NPs) with ZnFe 2 O 4 @Pt cores and glucose oxidase (GOx) shells. The ZFPG NPs possess five-enzyme activities, good sonosensitivity, and remarkable magnetic targeting properties, which facilitate sono-metallo-immunotherapy for prostate cancer treatment in male mice. Specifically, the magnetic targeting ability effectively improves their accumulation in tumors while still showing enrichment in the liver and kidneys. The multienzyme cascade catalysis and sonosensitivity of these NPs effectively deplete glutathione and glucose, and enhance the generation and utilization of H 2 O 2 , thereby inducing multiple ROS bursts. Furthermore, these comprehensive effects up-regulate the HMOX1 to promote the Fe 2+ and lipid peroxides accumulation, thereby inducing immunogenic ferroptosis. This strategy facilitates anti-tumor immunity by ameliorating the immunosuppressive TME and inhibiting lung metastatic progression. This joint warfare strategy offers a powerful solution to address conventional immunotherapy limitations.

研究领域: 纳米技术 · 癌症免疫治疗 · 生物医学工程 · 分子生物学 · 肿瘤学
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JOURNAL OF CONTROLLED RELEASE · 2021 · IF 9.776

Smart biomimetic metal organic frameworks based on ROS-ferroptosis-glycolysis regulation for enhanced tumor chemo-immunotherapy

Jie Yang,Siyu Ma,Rui Xu,Yawen Wei,Jun Zhang,Tiantian Zuo,Zhihua Wang,Huizi Deng,Ning Yang,Qi Shen

Antitumor immunotherapy is limited by low tumor immunogenicity and immunosuppressive microenvironment (TIME), which could be improved by “ROS-ferroptosis-glycolysis regulation” strategy. Herein, a cancer cell membrane coated metal organic framework (MOF) loading with glucose oxidase (GOx) and doxorubicin (DOX) was constructed (denoted as mFe(SS)/DG). Benefiting from the homotypic targeting of cancer cell membrane, the nanoplatform effectively accumulated in tumors. mFe(SS)/DG based on coordination between Fe 3+ and disulfide-bearing ligand scavenged GSH and downregulated glutathione peroxide 4 (GPX4) to trigger ferroptosis. GOx catalyzed glucose to generate abundant H 2 O 2 for enhancing Fenton reaction, resulting in excessive ROS in tumors. The ROS burst simultaneously promoted ferroptosis and inhibited glycolysis. Ferroptosis combined with DOX induced immunogenic cell death (ICD) and released tumor antigens to initiate antitumor immunity. Glycolysis repression remodeled TIME by decreasing lactate to solidify and boost the antitumor immunity. The smart biomimetic nanoplatform integrates tumor metabolism and immunity based on ROS-ferroptosis-glycolysis regulation, providing a potential anti-tumor strategy.

CAS / MDL: 505-73-7 10025-77-1
研究领域: 癌症研究 · 纳米技术 · 免疫疗法 · 生物化学 · 药学
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