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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]

Silver nanoparticles (AgNPs) have become widespread in the environment with increasing industrial applications. But the studies about their potential health risks are far from enough, especially in neurotoxic effects. This study aimed to investigate the neurotoxic effects of longer‐term exposure (prolonged exposure for 48 h and chronic exposure for 6 days) of 20nm AgNPs with/without polyvinylpyrrolidone (PVP) coating at low concentrations (0.01–10 mg·L−1) to Caenorhabditis elegans. The results suggested that exposure to AgNPs induced damage to nematode survival, with the longest and relative average life span reduced. Exposure to AgNPs caused neurotoxicity on locomotion behaviors (head thrashes, body bends, pharyngeal pumping frequency, and defecation interval) and sensory perception behaviors (chemotaxis assay and thermotaxis assay), as well as impaired dopaminergic, GABAergic, and cholinergic neurons, except for glutamatergic, based on the alters fluorescence intensity, in a dose‐ and time‐dependent manner. Further investigations suggested that the low‐dose AgNPs (0.01–0.1 mg·L−1) exposure raises receptors of GABAergic and dopamine in C. elegans at the genetic level, whereas opposite results were observed at higher doses (1–10 mg·L−1), which implied that AgNPs could cause neurotoxicity by impairing neurotransmitter delivery. The PVP‐AgNPs could cause a higher fatality rate and neurotoxicity at the same dose. Notably, AgNPs did not cause any deleterious effect on nematodes at the lowest dose of 0.01 mg·L−1. In general, these results suggested that AgNPs possess the neurotoxic potential in C. elegans and provided useful information to understand the neurotoxicity of AgNPs, which would offer an inspiring perspective on the safe application. In this study, C. elegans was used as a model to evaluate the neurotoxicity of longer‐term exposure of 20nm AgNPs with/without PVP coating at low concentrations. The decreased survival rate and damaged neurobehavior, as well as impaired neurons and neurotransmitters in C. elegans, were observed. The PVP‐AgNPs caused a higher fatality rate and neurotoxicity. The results indicated that AgNPs caused neurotoxicity on nematodes at the doses over 0.1 mg·L−1, which provided clues for the safe application of AgNPs. [ABSTRACT FROM AUTHOR]