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Silver nanoparticles (AgNPs) are widely used in many commercial and medical products. Serious concerns are paid on their adverse potentials to the environment and human health. In this study, toxic effects and oxidative stress induced by AgNPs with different sizes and coatings (20 nm AgNPs, 20 nm polyvinylpyrrolidone (PVP) -AgNPs and 50 nm AgNPs) in Caenorhabditis elegans (C. elegans) were investigated. The toxic effects including the shortened lifespan and decreased frequency of head thrashes and body bends of C. elegans were induced in a dose-dependent manner by AgNPs. The reactive oxygen species (ROS) production and the oxidative stress-related indicators including malondialdehyde (MDA) and glutathione (GSH) in nematodes were changed after exposure to three kinds of AgNPs. These effects were the most obvious in a 20 nm PVP-AgNPs exposure group. AgNPs could also induce the expression of genes related to oxidative stress in nematodes. In addition, the up-regulation of mtl-1 and mtl-2 in nematodes might reduce the oxidative damage caused by AgNPs, by using transgenic strains CF2222 and CL2120 nematodes. Metallothionein (MT), an antioxidant, could relieve the oxidative damage caused by AgNPs. These results suggested that 20 nm PVP-AgNPs with a smaller particle size and better dispersion have stronger toxic effects and the oxidative damage to nematodes. Mtl-1 and mtl-2 might be involved in alleviating the oxidative damage caused by AgNPs. Our findings provide clues for the safety evaluation and mechanism information of metal nanoparticles. Graphical Abstract [ABSTRACT FROM AUTHOR]

Recombinant human metallothionein III (rh‐MT‐III) is a genetically engineered product produced by Escherichia coli fermentation technology. Its molecules contain abundant reducing sulfhydryl groups, which possess the ability to bind heavy metal ions. The present study was to evaluate the binding effects of rh‐MT‐III against copper and cadmium in vitro and to investigate the antioxidant activity of rh‐MT‐III using Caenorhabditis elegans in vivo. For in vitro experiments, the binding rates of copper and cadmium were 91.4% and 97.3% for rh‐MT‐III at a dosage of 200 μg/mL at 10 h, respectively. For in vivo assays, the oxidative stress induced by copper (CuSO4, 10 μg/mL) and cadmium (CdCl2, 10 μg/mL) was significantly reduced after 72 h of exposure to different doses of rh‐MT‐III (5–500 μg/mL), indicated by restoring locomotion behavior and growth, and reducing malondialdehyde and reactive oxygen species levels in C. elegans. Moreover, rh‐MT‐III decreased the deposition of lipofuscin and fat content, which could delay the progression of aging. In addition, rh‐MT‐III (500 μg/mL) promoted the up‐regulation of Mtl‐1 and Mtl‐2 gene expression in C. elegans, which could enhance the resistance to oxidative stress by increasing the enzymatic activity of antioxidant defense system and scavenging free radicals. The results indicated that supplemental rh‐MT‐III could effectively protect C. elegans from heavy metal stress, providing an experimental basis for the future application and development of rh‐MT‐III. Rh‐MT‐III is a genetically engineered product fermented by Escherichia coli. This study evaluated the binding effects of rh‐MT‐III against copper and cadmium and the antioxidant activity of rh‐MT‐III in Caenorhabditis elegans. The data showed that rh‐MT‐III had high affinity for copper and cadmium and enhanced the stress resistance of nematodes by increasing the enzymatic activity of antioxidant defense system and scavenging free radicals. The results indicated that rh‐MT‐III could be used as an antioxidant to protect organisms from oxidative damage. [ABSTRACT FROM AUTHOR]

Microplastics have become a serious environmental pollutant and subsequently have harmful effects on human health. Thus, the impacts of microplastics on human cells need to be explored. In the present study, the cytotoxic effects at the subcellular-organelle levels to polystyrene nanoplastics (PS-NPs, diameter 21.5 ± 2.7 nm) were investigated in the human hepatocellular carcinoma (HepG2) cell line. The cell viability exposed to PS-NPs at the concentrations of 6.25, 12.5, 25 and 50 μg/mL for 24 h diminished in a concentration-dependent manner. The PS-NPs treatment induced mitochondrial injuries, including morphological changes, decreased adenosine triphosphate (ATP) production and the loss of mitochondrial membrane potentials (MMP). The PS-NPs treatment could further spark cell apoptosis by upregulating caspase 3, caspase 9, cytochrome c , and Bcl-2 associated X protein (Bax)/B-cell lymphoma-2 (Bcl-2) in HepG2 cells, which is related to the mitochondrial dysfunction. PS-NPs exposure stimulated the excessive cellular reactive oxygen species (ROS) production and also induced mitochondrial fission by upregulating dynamin-related protein 1 (DRP1) and P-DRP1, but downregulating optic atrophy protein 1 (OPA1) and peroxisome proliferator-activated receptor-gamma coactivator-1alpha (PGC-1α) expression levels. The above effects on mitochondria damage induced by PS-NPs were reversed by the pretreatment of N-acetylcysteine (NAC), mitochondrial division inhibitor 1 (Mdivi-1) and DRP1 siRNA. The results suggested that the interaction between ROS and DRP1-dependent mitochondrial division could promote mitochondrial lesions and mitochondria-related apoptosis caused by PS-NPs. These findings on molecular mechanisms provide a theoretical basis for preventing the hazards caused by microplastics to human health. [Display omitted] • PS-NPs decreased viability of HepG2 cells in a concentration-dependent manner. • PS-NPs induced oxidative stress and apoptosis in HepG2 cells. • PS-NPs induced mitochondrial morphological, function, dynamics injury in HepG2 cells. • NAC alleviated PS-NPs-induced cytotoxicity and mitochondrial injury. • Mdivi-1 and DRP1 siRNA relieved PS-NPs-induced cytotoxicity mitochondrial injury. [ABSTRACT FROM AUTHOR]