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Iron is vital for many physiological functions, including energy production, and dysregulated iron homeostasis underlies a number of pathologies. Ferroptosis is a recently recognized form of regulated cell death that is characterized by iron dependency and lipid peroxidation, and this process has been reported to be involved in multiple diseases. The mechanisms underlying ferroptosis are complex, and involve both well-described pathways (including the iron-induced Fenton reaction, impaired antioxidant capacity, and mitochondrial dysfunction) and novel interactions linked to cellular energy production. In this review, we examine the contribution of iron to diverse metabolic activities and their relationship to ferroptosis. There is an emphasis on the role of iron in driving energy production and its link to ferroptosis under both physiological and pathological conditions. In conclusion, excess reactive oxygen species production driven by disordered iron metabolism, which induces Fenton reaction and/or impairs mitochondrial function and energy metabolism, is a key inducer of ferroptosis.

As an emerging pollutant in the life cycle of plastic products, micro/nanoplastics (M/NPs) are increasingly being released into the natural environment. Substantial concerns have been raised regarding the environmental and health impacts of M/NPs. Although diverse M/NPs have been detected in natural environment, most of them display two similar features, i.e.,high surface area and strong binding affinity, which enable extensive interactions between M/NPs and surrounding substances. This results in the formation of coronas, including eco-coronas and bio-coronas, on the plastic surface in different media. In real exposure scenarios, corona formation on M/NPs is inevitable and often displays variable and complex structures. The surface coronas have been found to impact the transportation, uptake, distribution, biotransformation and toxicity of particulates. Different from conventional toxins, packages on M/NPs rather than bare particles are more dangerous. We, therefore, recommend seriously consideration of the role of surface coronas in safety assessments. This review summarizes recent progress on the eco–coronas and bio-coronas of M/NPs, and further discusses the analytical methods to interpret corona structures, highlights the impacts of the corona on toxicity and provides future perspectives.

The biotransformation of nanoparticles plays a crucial role in determining their biological fate and responses. Although a few engineering strategies (e.g., surface functionalization and shape control) have been employed to regulate the fate of nanoparticles, the genetic control of nanoparticle biotransformation remains an unexplored avenue. Herein, we utilized a CRISPR-based genome-scale knockout approach to identify genes involved in the biotransformation of rare earth oxide (REO) nanoparticles. We found that the biotransformation of REOs in lysosomes could be genetically controlled via SMPD1. Specifically, suppression of SMPD1 inhibited the transformation of La 2 O 3 into sea urchin-shaped structures, thereby protecting against lysosomal damage, proinflammatory cytokine release, pyroptosis and RE-induced pneumoconiosis. Overall, our study provides insight into how to control the biological fate of nanomaterials. Here the authors show that the biological fate of rare earth nanoparticles can be genetically controlled by SMPD1 in cells, offering insights for the prevention or treatment of rare earth associated hazard effects, such as inflammation and pneumoconiosis.

Sustainable developments of nanotechnology necessitate the exploration of structure-activity relationships (SARs) at nano-bio interfaces. While ferroptosis may contribute in the developments of some severe diseases (e.g., Parkinson’s disease, stroke and tumors), the cellular pathways and nano-SARs are rarely explored in diseases elicited by nano-sized ferroptosis inducers. Here we find that WS 2 and MoS 2 nanosheets induce an iron-dependent cell death, ferroptosis in epithelial (BEAS-2B) and macrophage (THP-1) cells, evidenced by the suppression of glutathione peroxidase 4 (GPX4), oxygen radical generation and lipid peroxidation. Notably, nano-SAR analysis of 20 transition metal dichalcogenides (TMDs) disclosures the decisive role of surface vacancy in ferroptosis. We therefore develop methanol and sulfide passivation as safe design approaches for TMD nanosheets. These findings are validated in animal lungs by oropharyngeal aspiration of TMD nanosheets. Overall, our study highlights the key cellular events as well as nano-SARs in TMD-induced ferroptosis, which may facilitate the safe design of nanoproducts. It is unclear whether 2D metal dichalcogenides (TMD) alone can cause ferroptotic cell death. Here, the authors show TMD nanosheets induced ferroptosis in mammalian cell lines and in a mouse model after aspiration of TMD materials into lungs, causing ferroptotic cell death.

While hypoxia promotes carcinogenesis, tumour aggressiveness, metastasis, and resistance to oncological treatments, the impacts of hyperoxia on tumours are rarely explored because providing a long-lasting oxygen supply in vivo is a major challenge. Herein, we construct micro oxygen factories, namely, photosynthesis microcapsules (PMCs), by encapsulation of acquired cyanobacteria and upconversion nanoparticles in alginate microcapsules. This system enables a long-lasting oxygen supply through the conversion of external radiation into red-wavelength emissions for photosynthesis in cyanobacteria. PMC treatment suppresses the NF-kB pathway, HIF-1α production and cancer cell proliferation. Hyperoxic microenvironment created by an in vivo PMC implant inhibits hepatocarcinoma growth and metastasis and has synergistic effects together with anti-PD-1 in breast cancer. The engineering oxygen factories offer potential for tumour biology studies in hyperoxic microenvironments and inspire the exploration of oncological treatments. Tumour hypoxia is an important factor in tumorigenesis and cancer therapy. Here, the authors present a micro oxygenation factory, capable of providing an oxygen supply through photosynthesis, and demonstrate its utility in cancer therapy.

Increasing concerns over the possible risks of nanotechnology necessitates breakthroughs in structure–activity relationship (SAR) analyses of engineered nanomaterials (ENMs) at nano-bio interfaces. However, current nano-SARs are often based on univariate assessments and fail to provide tiered views on ENM-induced bio-effects. Here we report a multi-hierarchical nano-SAR assessment for a representative ENM, Fe 2 O 3 , by metabolomics and proteomics analyses. The established nano-SAR profile allows the visualizing of the contributions of seven basic properties of Fe 2 O 3 to its diverse bio-effects. For instance, although surface reactivity is responsible for Fe 2 O 3 -induced cell migration, the inflammatory effects of Fe 2 O 3 are determined by aspect ratio (nanorods) or surface reactivity (nanoplates). These nano-SARs are examined in THP-1 cells and animal lungs, which allow us to decipher the detailed mechanisms including NLRP3 inflammasome pathway and monocyte chemoattractant protein-1-dependent signaling. This study provides more insights for nano-SARs, and may facilitate the tailored design of ENMs to render them desired bio-effects. Understanding nano-bio interactions is key to optimizing the biocompatible design of nanomaterials. Here, the authors combine proteomic and metabolomics studies to evaluate the effect of varying physicochemical properties of iron oxide nanoparticles in macrophage-like cells and mouse lungs.

Concerns regarding chronic injuries ( e.g ., fibrosis and carcinogenesis) induced by nanoparticles raised public health concerns and need to be rapidly assessed in hazard identification. Although in silico analysis is commonly used for risk assessment of chemicals, predicting chronic in vivo nanotoxicity remains challenging due to the intricate interactions at multiple interfaces like nano-biofluids and nano-subcellular organelles. Herein, we develop a multimodal feature fusion analysis framework to predict the fibrogenic potential of metal oxide nanoparticles (MeONPs) in female mice. Treating each nano-bio interface as an independent entity, eighty-seven features derived from MeONP-lung interactions are used to develop a machine learning-based predictive framework for lung fibrosis. We identify cell damage and cytokine (IL-1β and TGF-β1) production in macrophages and epithelial cells as key events closely associated with particle size, surface charge, and lysosome interactions. Experimental validations show that the developed in silico model has 85% accuracy. Our findings demonstrate the potential usefulness of this predictive model for risk assessment of nanomaterials and in assisting regulatory decision-making. While the model is developed based on 52 MeONPs, further validation using a larger nanoparticle library is necessary to confirm its broader applicability. The prediction of chronic toxicity is a major challenge in nanotoxicity studies. Here, the authors present an in silico framework for predicting ENM-induced lung fibrosis, displaying 85% accuracy in experimental validation and leading to identification of key events at nano-bio interfaces that allows mechanism interpretation of ENM-induced lung fibrosis.

Image dehazing is a vital research area in computer vision. Many existing deep learning-based dehazing methods rely on atmospheric scattering models with manually predefined, non-trainable parameters, which limits their adaptability and transferability. We propose Alpha-DehazeNet, a novel model that leverages red green blue alpha (RGBA) haze layer effect maps by defining a grayscale transparency map in the RGBA color space as the initial haze layer. Alpha-DehazeNet employs a U-Net generator enhanced with a spatial attention mechanism to encode haze-related features. This generator is integrated into an adversarial architecture with residual connections, enabling end-to-end training. Additionally, a depth consistency loss is introduced to improve dehazing accuracy. Alpha-DehazeNet outperforms several state-of-the-art models on synthetic datasets (ITS and OTS from RESIDE), achieving 37.35 dB peak signal-to-noise ratio (PSNR) on SOTS-indoor and 37.39 dB PSNR on SOTS-outdoor, while using only 8.86 million parameters. On real-world datasets, Alpha-DehazeNet delivers competitive results, although it shows limitations in handling non-white fog and cloud conditions. The code is publicly available at: https://doi.org/10.5281/zenodo.15361810 .

To study the autonomous walking performance and corresponding electromechanical characteristics of unmanned mining equipment under different slopes, turning radii, and ground conditions. Firstly, the autonomous walking systems based on PID, fuzzy PID, and BP PID, in this paper, are constructed, and then the electromechanical coupling simulation is carried out to analyse autonomous walking performance and electromechanical characteristics of mining double-track chassis under different working conditions. Finally, the feasibility of the autonomous walking system based on fuzzy PID is verified by the path-tracking experiment. The results show that the autonomous walking performance of the autonomous walking system based on the fuzzy PID is the best. Under the soft ground, the current, voltage, and load torque are all increased to varying degrees due to the sinking phenomenon of the crawler, but the driving speed is reduced, and when mining double-track chassis makes large-radius turns, the autonomous walking system based on the BP PID can also be given priority with a path deviation within 0.1 m.

Ferroptosis is a promising strategy for cancer therapy, with numerous inhibitors of its braking axes under investigation as potential drugs. However, few studies have explored the potential of activating the driving axes to induce ferroptosis. Herein, phosphatidylcholine peroxide decorating liposomes (LIP PCPO ) are synthesized to induce ferroptosis by targeting divalent metal transporter 1 (DMT1). LIP PCPO is found to boost lysosomal Fe 2+ efflux by inducing cysteinylation of lysosomal DMT1, resulting in glutathione peroxidase 4 (GPX4) suppression, glutathione depletion and ferroptosis in breast cancer cells and xenografts. Importantly, LIP PCPO induced ferroptotic cell death is independent of acquired resistance to radiation, chemotherapy, or targeted agents in 11 cancer cell lines. Furthermore, a strong synergistic ferroptosis effect is observed between LIP PCPO and an FDA-approved drug, artesunate, as well as X rays. The formula of LIP PCPO encapsulating artesunate significantly inhibits tumor growth and metastasis and improves the survival rate of breast cancer-bearing female mice. These findings provide a distinct strategy for inducing ferroptosis and highlight the potential of LIP PCPO as a vector to synergize the therapeutic effects of conventional ferroptosis inducers. Inducers of ferroptosis hold potential for cancer therapy. Here, the authors identify a peroxide-decorated liposome capable of inducing ferroptosis and enhancing the efficacy of chemotherapeutic agents and radiotherapy.