Antimony trioxide nanoparticles promote ferroptosis in developing zebrafish (Danio rerio) by disrupting iron homeostasis.

The widespread use of antimony trioxide (ATO) and ATO nanoparticles (nATO) has led to increasing ecological and health risks. However, there is relatively insufficient research on the aquatic ecotoxicology of nATO. This study revealed that nATO affects the development of zebrafish embryos and mainly induces ferroptosis through the dissolution of Sb(III). The size of nATO ranged from 50 to 250 nm, and it generated free radicals in water. It can be ingested and accumulate in zebrafish larvae and affects normal development. Compared with those in the control group, the levels of reactive oxygen species (ROS), cell apoptosis, mitochondrial damage and iron content in the group exposed to high concentrations of nATO were increased. The transcriptomics results indicated that nATO significantly altered the expression levels of key genes related to glutathione metabolism and ferroptosis. Quantitative polymerase chain reaction consistently demonstrated the reliability of the transcriptome data and revealed that nATO induced ferroptosis by disrupting iron homeostasis and the key factor is the dissolution of Sb(III). Furthermore, ferrostatin-1, an inhibitor of ferroptosis, decreased the levels of ROS, apoptosis and mitochondrial damage induced by nATO, which further prove that nATO can promote ferroptosis. This work deepens the understanding of the ecological toxicological effects of nATO in aquatic environments and its mechanisms, which is highly important for the development of antimony management strategies.

Toxicity and related molecular mechanisms of Sb(III) in the embryos and larvae of zebrafish (Danio rerio).

Antimony (Sb) pollution poses a severe threat to humans and ecosystems due to the extensive use of Sb in various fields. However, little is known about the toxic effects of Sb and its aquatic ecotoxicological mechanism. This study aimed to reveal the toxicity and related molecular mechanisms of trivalent Sb (Sb(III)) in zebrafish embryos/larvae. Sb(III) accumulated in larvae, which correlated with the exposure concentration. Although no significant lethal or teratogenic effects were observed, normal growth and development were affected. Exposure to 10 or 20 mg/L Sb(III) increased the levels of reactive oxygen species in the larvae while enhancing catalase activity and increasing cell apoptosis. Transcriptomic analysis revealed that Sb(III) promoted glutathione metabolism and the ferroptosis pathway. In addition, symptoms associated with ferroptosis, including mitochondrial damage, biochemical levels of related molecules and increased tissue iron content, were detected. Quantitative polymerase chain reaction (qPCR) analyses further confirmed that Sb(III) significantly altered the transcription levels of genes related to the ferroptosis pathway by disrupting iron homeostasis. Furthermore, ferrostatin-1 (Fer-1) mitigated the toxic effects induced by Sb(III) in zebrafish. Our research fills the gap in the literature on the toxicity and mechanism of Sb(III) in aquatic organisms, which is highly important for understanding the ecological risks associated with Sb.

Interactions of antimony with biomolecules and its effects on human health.

Antimony (Sb) pollution has increased health risks to humans as a result of extensive application in diverse fields. Exposure to different levels of Sb and its compounds will directly or indirectly affect the normal function of the human body, whereas limited human health data and simulation studies delay the understanding of this element. In this review, we summarize current research on the effects of Sb on human health from different perspectives. First, the exposure pathways, concentration and excretion of Sb in humans are briefly introduced, and several studies have revealed that human exposure to high levels of Sb will cause higher concentrations in body tissues. Second, interactions between Sb and biomolecules or other nonbiomolecules affected biochemical processes such as gene expression and hormone secretion, which are vital for causing and understanding health effects and mechanisms. Finally, we discuss the different health effects of Sb at the biological level from small molecules to individual. In conclusion, exposure to high levels of Sb compounds will increase the risk of disease by affecting different cell signaling pathways. In addition, the appropriate form and dose of Sb contribute to inhibit the development of specific diseases. Key challenges and gaps in toxicity or benefit effects and mechanisms that still hinder risk assessment of human health are also identified in this review. Systematic studies on the relationships between the biochemical process of Sb and human health are needed.

Native nanodiscs from blood inhibit pulmonary fibrosis.

Blood is a treasure trove whose constituents have attracted increasing attention for use in understanding and controlling disease. However, the functions of blood, especially with regard to its composition at the nanoscale, remain largely unknown. Inspired by exosomes and lipoproteins, the present work isolated and characterized biotic nanodiscs from human blood (BNHBs) using multiple techniques. The isolated BNHBs had diameters of 10-30 nm and a thicknesses of approximately 2.9 nm. The BNHB concentration in blood peaked at 34.5 ±â€¯5.19 mg/mL (20-fold higher than that of high-density lipoproteins and exosomes). BNHBs had high biocompatibility, facile cell internalization and strong biological control of pulmonary fibrosis. The BNHBs were hybrids of many metalloproteins and metabolites and contained a few functional proteins similar to lipoproteins or exosomal proteins. BNHBs inhibited transforming growth factor-beta 1 (TGF-ß1)-induced fibrosis damage in human embryonic lung fibroblasts (HELFs) by inhibiting the expression of α-smooth muscle actin and collagen-1 protein. BNHBs also intensively bound TGF-ß1 to inhibit TGF-ß1 activity in fibrogenesis. BNHBs successfully reduced pulmonary inflammation and collagen deposition in a mouse model, preventing pulmonary fibrosis. Applying the protective properties of nanodiscs may be a novel therapeutic approach for pulmonary and other diseases.

Graphene Oxide Inhibits Antibiotic Uptake and Antibiotic Resistance Gene Propagation.

Antibiotics and antibiotic resistance genes (ARGs) in the natural environment have become substantial threats to the ecosystem and public health. Effective strategies to control antibiotics and ARG contaminations are emergent. A novel carbon nanomaterial, graphene oxide (GO), has attracted a substantial amount of attention in environmental fields. This study discovered the inhibition effects of GO on sulfamethoxazole (SMZ) uptake for bacteria and ARG transfer among microorganisms. GO promoted the penetration of SMZ from intracellular to extracellular environments by increasing the cell membrane permeability. In addition, the formation of a GO-SMZ complex reduced the uptake of SMZ in bacteria. Moreover, GO decreased the abundance of the sulI and intI genes by approximately 2-3 orders of magnitude, but the global bacterial activity was not obviously inhibited. A class I integron transfer experiment showed that the transfer frequency was up to 55-fold higher in the control than that of the GO-treated groups. Genetic methylation levels were not significant while sulI gene replication was inhibited. The biological properties of ARGs were altered due to the GO-ARG noncovalent combination, which was confirmed using multiple spectral analyses. This work suggests that GO can potentially be applied for controlling ARG contamination via inhibiting antibiotic uptake and ARG propagation.