Results of a 30-day safety assessment in young mice orally exposed to polystyrene nanoparticles.

Polystyrene nanoparticles (PSNPs) are a newly emerging pollutant in the natural environment. However, due to the lack of sufficient toxicological studies in mammals, the potential effects of PSNPs on human health remain largely undefined. Therefore, in this study, young mice aged four weeks old were subjected to oral administration of 0, 0.2, 1, or 10 mg/kg PSNPs for 30 days. Our results demonstrated for the first time that oral exposure to PSNPs affected the expressions of mucus secretion-related genes and altered the community composition of intestinal microbiota, although this treatment did not cause behavioral impairments in young mice. No significant alterations in inflammatory or oxidative stress-related indicators were observed in the liver, lung, intestine, cortex or serum of PSNPs-treated animals. Moreover, exposure to PSNPs did not cause pathological changes in the liver, lung, or cortex tissues. Notably, although oral administration of PSNPs did not produce obvious toxic effects in the major organs of young mice, the possible toxicity of PSNPs remains unresolved and it may depend on the dose, exposure route and species. The potential hazardous effects of PSNPs still need to be systematically assessed, especially for children who are susceptible to exposure to nanoparticles.

Autophagy deficiency exacerbates acute lung injury induced by copper oxide nanoparticles.

Copper oxide nanoparticles (CuONPs) are one of the widely used metal nanoparticles in the industrial and commercial fields. Autophagy is an intracellular degradation system that delivers cytoplasmic constituents to the lysosome and has been linked to nanoparticles-induced toxicity. In particular, the roles of autophagy in response to CuONPs have been explored in vitro, although the conclusions are controversial. To clarify the role of autophagy in CuONPs-induced acute lung injury, microtubule-associated protein 1 light chain 3 beta (Map1lc3b or lc3b) knockout mice and their corresponding wild type mice are applied. Our results showed that single-dose intratracheal instillation of CuONPs with dosages of 1.25, 2.5 or 5 mg/kg caused acute lung injury 3 days after treatment in a dose-dependent manner, as evidenced by deteriorative lung histopathology, more infiltration of macrophage cells, increased oxidative stress and copper ions. Loss of lc3b resulted in aggravated lung injury induced by CuONPs, which was probably due to the blockade of mitophagy and consequently the accumulation of aberrant mitochondria with overloaded copper ions. Our study provides the first in vivo evidence that autophagy deficiency exacerbates CuONPs-induced acute lung injury, and highlights that targeting autophagy is a meaningful strategy against CuONPs-associated respiratory toxicity.

Arsenite induces ferroptosis in the neuronal cells via activation of ferritinophagy.

Ferroptosis is a novel form of cell death that involves in the pathophysiological process of diverse brain diseases. However, how arsenite induces ferroptosis in the neuronal cells remains unsolved. In this study, by using in vitro and in vivo models, we demonstrated that arsenite was able to trigger ferroptosis in the neuronal cells. Exposure of arsenite for 6 months at 0.5, 5 and 50 mg/L arsenite via drinking water significantly reduced the number of neurons and caused the pathological changes in the mitochondria of hippocampus. Treatment of arsenite elevated the contents of lipid peroxidation products, disrupted the iron homeostasis, altered the expressions of ferroptosis-related proteins in the hippocampus and PC-12 cells. The results also showed that arsenite significantly decreased the expressions of ferritin and NCOA4, but sharply enhanced the level of autophagy marker LC3B, suggesting the activation of ferritinophagy by arsenite. Co-treatment of arsenite with ferroptosis inhibitor ferrostatin-1, or autophagy inhibitors 3-MA and BafA1, all remarkably attenuated the cytotoxic effects of arsenite. These findings not only present a novel mechanism that arsenite triggers ferroptosis in the neuronal cells via activation of ferritinophagy, but also indicate that regulating ferritinophagy to control iron level may provide a clue for prevention against arsenite neurotoxicity.

Type-II Interface Band Alignment in the vdW PbI2-MoSe2 Heterostructure.

Energy band alignments at heterostructure interfaces play key roles in device performance, especially between two-dimensional atomically thin materials. Herein, van der Waals PbI2-MoSe2 heterostructures fabricated by in situ PbI2 deposition on monolayer MoSe2 are comprehensively studied using scanning tunneling microscopy/spectroscopy, atomic force microscopy, photoemission spectroscopy, and Raman and photoluminescence (PL) spectroscopy. PbI2 grows on MoSe2 in a quasi layer-by-layer epitaxial mode. A type-II interface band alignment is proposed between PbI2 and MoSe2 with the conduction band minimum (valence band maximum) located at PbI2 (MoSe2), which is confirmed by first-principles calculations and the existence of interfacial excitons revealed using temperature-dependent PL. Our findings provide a scalable method to fabricate PbI2-MoSe2 heterostructures and new insights into the electronic structures for future device design.

PbI2-MoS2 Heterojunction: van der Waals Epitaxial Growth and Energy Band Alignment.

van der Waals (vdW) epitaxy offers a promising strategy without lattice and processing constraints to prepare atomically clean and electronically sharp interfaces for fundamental studies and electronic device demonstrations. Herein, PbI2 was thermally deposited at high-vacuum conditions onto CVD-grown monolayer MoS2 flakes in a vdW epitaxial manner to form 3D-2D heterojunctions, which are promising for vdW epitaxial growth of perovskite films. X-ray diffraction, X-ray photoemission spectroscopy, Raman, and atomic force microscopy measurements reveal the structural properties of the high-quality heterojunctions. Photoluminescence (PL) measurements reveal that the PL emissions from the bottom MoS2 flakes are greatly quenched compared to their as-grown counterparts, which can be ascribed to the band alignment-induced distinct interfacial charge-transfer behaviors. Strong interlayer excitons can be detected at the PbI2/MoS2 interface, indicating an effective type II band alignment, which can be further confirmed by ultraviolet photoemission spectroscopy measurements. The results provide a new material platform for the application of the vdW heterojunctions in electronic and optoelectronic devices.