The valence state of iron-based nanomaterials determines the ferroptosis potential in a zebrafish model

Zheng, Naying; Sun, Xiaolian; Shi, Yanyun; Chen, Luheng; Wang, Luanjin; Cai, Haoxing; Han, Changshun; Liao, Tingting; Yang, Chunyan; Zuo, Zhenghong; He, Chengyong

doi:10.1016/j.scitotenv.2022.158715

Cited by 13 publications

(4 citation statements)

References 52 publications

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“…The core chemistry, specifically, the valence state of iron-based nanomaterials, may also play a role in their ferroptosis potential [35]. Furthermore, the availability of Fe in the cells is important.…”

Section: Discussionmentioning

confidence: 99%

High-Dose Exposure to Polymer-Coated Iron Oxide Nanoparticles Elicits Autophagy-Dependent Ferroptosis in Susceptible Cancer Cells

Lomphithak,

Helvacioglu,

Armenia

et al. 2023

Nanomaterials

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Ferroptosis, a form of iron-dependent, lipid peroxidation-driven cell death, has been extensively investigated in recent years, and several studies have suggested that the ferroptosis-inducing properties of iron-containing nanomaterials could be harnessed for cancer treatment. Here we evaluated the potential cytotoxicity of iron oxide nanoparticles, with and without cobalt functionalization (Fe2O3 and Fe2O3@Co-PEG), using an established, ferroptosis-sensitive fibrosarcoma cell line (HT1080) and a normal fibroblast cell line (BJ). In addition, we evaluated poly (ethylene glycol) (PEG)-poly(lactic-co-glycolic acid) (PLGA)-coated iron oxide nanoparticles (Fe3O4-PEG-PLGA). Our results showed that all the nanoparticles tested were essentially non-cytotoxic at concentrations up to 100 μg/mL. However, when the cells were exposed to higher concentrations (200–400 μg/mL), cell death with features of ferroptosis was observed, and this was more pronounced for the Co-functionalized nanoparticles. Furthermore, evidence was provided that the cell death triggered by the nanoparticles was autophagy-dependent. Taken together, the exposure to high concentrations of polymer-coated iron oxide nanoparticles triggers ferroptosis in susceptible human cancer cells.

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Section: Discussionmentioning

confidence: 99%

High-Dose Exposure to Polymer-Coated Iron Oxide Nanoparticles Elicits Autophagy-Dependent Ferroptosis in Susceptible Cancer Cells

Lomphithak,

Helvacioglu,

Armenia

et al. 2023

Nanomaterials

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“…At 60 and 72 hpf, the rates of hatching and mortality were evaluated. The calculation method is based on previous studies, and the following formula was adopted [ 18 ]: Mortality rate (%) = (deathed embryo number/total embryo number) × 100%. Hatching rate (%) = (hatched embryo number/total embryo number) × 100%…”

Section: Methodsmentioning

confidence: 99%

Esketamine Exposure Impairs Cardiac Development and Function in Zebrafish Larvae

Huang,

Wang,

Lin

et al. 2024

Toxics

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Esketamine is a widely used intravenous general anesthetic. However, its safety, particularly its effects on the heart, is not fully understood. In this study, we investigated the effects of esketamine exposure on zebrafish embryonic heart development. Zebrafish embryos were exposed to esketamine at concentrations of 1, 10, and 100 mg/L from 48 h post-fertilization (hpf) to 72 hpf. We found that after exposure, zebrafish embryos had an increased hatching rate, decreased heart rate, stroke volume, and cardiac output. When we exposed transgenic zebrafish of the Tg(cmlc2:EGFP) strain to esketamine, we observed ventricular dilation and thickening of atrial walls in developing embryos. Additionally, we further discovered the abnormal expression of genes associated with cardiac development, including nkx2.5, gata4, tbx5, and myh6, calcium signaling pathways, namely ryr2a, ryr2b, atp2a2a, atp2a2b, slc8a3, slc8a4a, and cacna1aa, as well as an increase in acetylcholine concentration. In conclusion, our findings suggest that esketamine may impair zebrafish larvae’s cardiac development and function by affecting acetylcholine concentration, resulting in weakened cardiac neural regulation and subsequent effects on cardiac function. The insights garnered from this research advocate for a comprehensive safety assessment of esketamine in clinical applications.

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“…In addition to neurotoxicity, ferroptosis can also impact reproductive health in fish. Zheng et al's study 46 observed that iron-based nanomaterials with different valences could induce ferroptosis, causing cardiac developmental defects in zebrafish, leading to enlarged ventricles or atria, depending on the valence state of the nanomaterials. The heart, as a crucial organ in reproductive function, is responsible for circulating reproductive hormones and oxygen to reproductive organs, and any malformation or dysfunction could lead to adverse reproductive outcomes.…”

Section: Mammalsmentioning

confidence: 99%

Ferroptosis Induced by Pollutants: An Emerging Mechanism in Environmental Toxicology

Yang,

Cai,

2024

Environ. Sci. Technol.

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Environmental pollutants have been recognized for their ability to induce various adverse outcomes in both the environment and human health, including inflammation, apoptosis, necrosis, pyroptosis, and autophagy. Understanding these biological mechanisms has played a crucial role in risk assessment and management efforts. However, the recent identification of ferroptosis as a form of programmed cell death has emerged as a critical mechanism underlying pollutant-induced toxicity. Numerous studies have demonstrated that fine particulates, heavy metals, and organic substances can trigger ferroptosis, which is closely intertwined with lipid, iron, and amino acid metabolism. Given the growing evidence linking ferroptosis to severe diseases such as heart failure, chronic obstructive pulmonary disease, liver injury, Parkinson's disease, Alzheimer's disease, and cancer, it is imperative to investigate the role of pollutant-induced ferroptosis. In this review, we comprehensively analyze various pollutant-induced ferroptosis pathways and intricate signaling molecules and elucidate their integration into the driving and braking axes. Furthermore, we discuss the potential hazards associated with pollutant-induced ferroptosis in various organs and four representative animal models. Finally, we provide an outlook on future research directions and strategies aimed at preventing pollutant-induced ferroptosis. By enhancing our understanding of this novel form of cell death and developing effective preventive measures, we can mitigate the adverse effects of environmental pollutants and safeguard human and environmental health.

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The valence state of iron-based nanomaterials determines the ferroptosis potential in a zebrafish model

Cited by 13 publications

References 52 publications

High-Dose Exposure to Polymer-Coated Iron Oxide Nanoparticles Elicits Autophagy-Dependent Ferroptosis in Susceptible Cancer Cells

High-Dose Exposure to Polymer-Coated Iron Oxide Nanoparticles Elicits Autophagy-Dependent Ferroptosis in Susceptible Cancer Cells

Esketamine Exposure Impairs Cardiac Development and Function in Zebrafish Larvae

Ferroptosis Induced by Pollutants: An Emerging Mechanism in Environmental Toxicology

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