Nonfullerene acceptors (NFAs) have played an important role in the development of organic solar cells. However, the optical absorption of most NFAs is limited within 600−900 nm, prohibiting further improvement of short-circuit current density (J sc ). To alleviate this problem, a fused-ring π-core BzS was designed by combining weakly electron-withdrawing benzotriazole (Bz) and strongly electron-donating selenophene together. Besides, the length of N-alkyl chain on the Bz moiety was engineered to tune the morphology, affording two NFAs mBzS-4F and EHBzS-4F. Both NFAs possess an absorption edge approaching 1000 nm, as resulted from the enhanced intramolecular charge transfer in conjunction with efficient intra-and intermolecular interactions. Binary photovoltaic devices based on PM6:mBzS-4F showed a power conversion efficiency of 17.02% with a very high J sc of 27.72 mA/cm 2 and a low energy loss of 0.446 eV. This work provides a strategy for future design of efficient NIR-responsive materials.

Plastic debris in the global biosphere is an increasing concern, and nanoplastic (NPs) toxicity in humans is far from being understood. Studies have indicated that NPs can affect mitochondria, but the underlying mechanisms remain unclear. The liver and lungs have important metabolic functions and are vulnerable to NP exposure. In this study, we investigated the effects of 80 nm NPs on mitochondrial functions and metabolic pathways in normal human hepatic (L02) cells and lung (BEAS-2B) cells. NP exposure did not induce mass cell death; however, transmission electron microscopy analysis showed that the NPs could enter the cells and cause mitochondrial damage, as evidenced by overproduction of mitochondrial reactive oxygen species, alterations in the mitochondrial membrane potential, and suppression of mitochondrial respiration. These alterations were observed at NP concentrations as low as 0.0125 mg/mL, which might be comparable to the environmental levels. Nontarget metabolomics confirmed that the most significantly impacted processes were mitochondrial-related. The metabolic function of L02 cells was more vulnerable to NP exposure than that of BEAS-2B cells, especially at low NP concentrations. This study identifies NP-induced mitochondrial dysfunction and metabolic toxicity pathways in target human cells, providing insight into the possibility of adverse outcomes in human health.

Triclosan (TCS), an extensively used antimicrobial agent, has raised considerable concern due to its hepatocarcinogenic potential. However, previous hepatotoxicity studies primarily focused on the activation of specific intracellular receptors, the underlying mechanisms still warrant further investigation at the metabolic level. Herein, we applied metabolomics in combination with lipidomics to unveil TCS-related metabolic responses in human normal and cancerous hepatocytes. Endogenous and exogenous metabolites were analyzed for the identification of metabolic biomarkers and biotransformation products. In L02 normal cells, TCS exposure induced the up-regulation of purine metabolism and amino acid metabolism, caused lipid accumulation, and disturbed energy metabolism. These metabolic disorders in turn enhanced the overproduction of reactive oxygen species (ROS), leading to the alteration of antioxidant enzyme activities, down-regulation of endogenous antioxidants, and peroxidation of lipids. TCS-induced oxidative stress is thus considered to be one crucial factor for hepatotoxicity. However, in HepG2 cancer cells, TCS underwent fast detoxification through phase II metabolism, accompanied by the enhancement of energy metabolism and elevation of antioxidant defense system, which contributed to the potential effects of TCS on human hepatocellular carcinoma development. These different responses of metabolism between normal and cancerous hepatocytes provide novel and robust perspectives for revealing the mechanisms of TCS-triggered hepatotoxicity.

Triclosan (TCS) and triclocarban (TCC) are widely used as bactericides in personal-care products. They are frequently found in environmental water and have the potential to cause a number of environmental and human health problems. In this study, we investigated adsorption and magnetic extraction for efficient removal of TCS and TCC from water and serum samples by core–shell structured magnetic covalent organic framework nanocomposites (Fe3O4@COFs). The as-prepared Fe3O4@COFs was fabricated on the Fe3O4 nanoparticles in situ growth strategy at room temperature via condensation reaction of 1,3,5-tris­(4-aminophenyl) benzene (TAPB) and terephthaldicarbox-aldehyde (TPA) in the presence of dimethyl sulfoxide (DMSO). The whole process of adsorption was monitored by ultrahigh performance liquid chromatography–tandem mass spectrometry (UHPLC-MS/MS) analysis with high sensitivity. The adsorption behaviors showed high adsorption capacity and fast adsorption. Furthermore, the adsorption performance through Langmuir and Freundlich isotherms showed multilayer adsorption through the interactions of space embedding effect, van der Waals forces, and benzene ring π–π stacking at a low concentration range and monolayer adsorption through strong π–π stacking at a high concentration range between the interface of TCS or TCC and Fe3O4@COFs at a high concentration range. Results indicated that the adsorption of TCS and TCC onto Fe3O4@COFs can be better represented by the pseudo-second-order model. Good removal efficiencies (82.3∼95.4%) and recoveries (92.9∼109.5%) of TCS and TCC in fetal bovine serum (FBS) and reusability at least 10 times were achieved. The Fe3O4@COFs exhibited high stability and excellent performance for the removal of TCS and TCC from water and biological samples. The results presented here thus reveal the exceptional potential of COFs for high-efficient environmental remediation.

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