Metabolomics reveals size-dependent persistence and reversibility of silver nanoparticles toxicity in freshwater algae.

Although the toxicity of silver nanoparticles (AgNPs) has been widely reported, the persistence and reversibility of AgNPs toxicity are poorly understood. In the present work, AgNPs with particle sizes of 5 nm, 20 nm, and 70 nm (AgNPs5, AgNPs20, and AgNPs70) were selected to investigate the nanotoxicity and recovery effects of Chlorella vulgaris in the exposure (72 h) and recovery (72 h) stages using non-targeted metabolomics techniques. The exposure of AgNPs exerted size-dependent effects on several aspects of C. vulgaris physiology, including growth inhibition, chlorophyll content, intracellular silver accumulation, and differential expression of metabolites, and most of these adverse effects were reversible. Metabolomics revealed that AgNPs with small sizes (AgNPs5 and AgNPs20) mainly inhibited glycerophospholipid and purine metabolism, and the effects were reversible. In contrast, AgNPs with large sizes (AgNPs70) reduced amino acid metabolism and protein synthesis by inhibiting aminoacyl-tRNA biosynthesis, and the effects were irreversible, demonstrating the persistence of nanotoxicity of AgNPs. The size-dependent persistence and reversibility of AgNPs toxicity provides new insights to further understand the mechanisms of toxicity of nanomaterials.

Post-traumatic cauda equina nerve calcification: A case report.

BACKGROUND: Post-traumatic cauda equina nerve calcification is extremely rare in clinical practice, and its etiology, pathogenesis, treatment and prognosis are unclear. There are few studies and reports on Post-traumatic cauda equina nerve calcification, and this review reports a case of Post-traumatic cauda equina nerve calcification for reference. CASE SUMMARY: A 52-year-old patient presented to our hospital with a history of lumbar spinal stenosis and a lumbar vertebral fracture caused by trauma. The patient's right lower limb had weakness in hip flexion, knee extension and plantarflexion with muscle strength grade 3, right ankle dorsiflexion and thumb dorsiflexion with muscle strength grade 0. The patient's skin sensation below the right knee plane disappeared. The patient's Computed tomography (CT) data showed signs of cauda equina nerve calcification and the terminal filaments in the plane of the third to fifth lumbar vertebrae. After treatment the patient's symptoms were slightly relieved. CONCLUSION: We provide an extremely rare case of Post-traumatic cauda equina nerve calcification and offer a conservative treatment plan. However, the etiology, mechanism and treatment of Post-traumatic cauda equina nerve calcification are still unclear. This requires scholars to conduct more research and exploration in this area.

Proteomic profiling reveals mitochondrial toxicity of nanosilver and silver nitrate in the gill of common carp.

Mitochondria are recognized as an important target organelle for the toxicity of nanomaterials. Although the toxic effects of silver nanoparticles (AgNPs) on mitochondria have been widely reported, the mechanism behind the toxicity remains unclear. In this study, the effects of two forms of silver (AgNPs and AgNO3) on carp gill mitochondria were investigated by analyzing the mitochondrial ultrastructure, physicochemical properties of mitochondrial membrane, and mitochondrial proteomics. After exposure of common carp to AgNPs (0.75 mg/L) and AgNO3 (0.05 mg/L) for 96 h, both forms of silver were shown to cause gill mitochondrial lesions, including irregular shape, loss of mitochondrial cristae, and increased mitochondrial membrane permeability. Proteomics results revealed that AgNPs and AgNO3 induced 362 and 297 differentially expressed proteins (DEPs) in gill mitochondria, respectively. Among the DEPs, 244 were shared between AgNPs and AgNO3 treatments. These shared proteins were mainly distributed in the mitochondrial membrane and matrix, and were significantly enriched in the tricarboxylic acid (TCA) cycle and oxidative phosphorylation pathway. The functional annotation of DEPs induced by both silver forms was mainly involved in energy production and conversion. These results indicated that the toxic mechanism of AgNPs and AgNO3 on gill mitochondria were comparable and the two forms of silver caused mitochondrial dysfunction in fish gills by inhibiting the TCA cycle and disrupting the electron transport chain.

Trophodynamics and health risk assessment of toxic trace metals in the food web of a plateau freshwater lake.

The trophodynamics of toxic trace metals is significant for assessing the threat of toxic trace metals to the aquatic ecosystem and human safety. However, due to the difficulty of accurately calculating the trophic positions of freshwater aquatic organisms in the food web, the comprehensive process of trophodynamics of toxic trace metals in freshwater ecosystems was still rarely known. By integrating the compound-specific nitrogen stable isotopic analysis of amino acids (CSIA-AAs) and the Bayesian stable isotope mixing model (SIMM) as a novel approach, the present study investigated the trophodynamics of five toxic trace metals (Zn, As, Cr, Cu, and Hg) in the food web of the YangZong Lake, a plateau freshwater lake that was once heavily polluted by arsenic in Yunnan Province, China. The results revealed that Hg tended to be efficiently biomagnified in the food web with a trophic magnification factor of 1.75; As, Cr, and Cu were biodiluted significantly, while Zn showed no biomagnification or biodilution trends. The dietary health risk assessment indicated the potential health risk of toxic trace metals for the local residents of long-term fish consumption. The present work highlights the accuracy and reliability of the novel CSIA-AAS+SIMM approach in the calculation of the trophic positions of freshwater organisms.

Metabolomics reveals the mechanism of polyethylene microplastic toxicity to Daphnia magna.

Microplastic exposure leads to various toxic effects in Daphnia magna; however, the effects of microplastics on the metabolic processes in D. magna and the corresponding molecular toxicity mechanisms remain unclear. In the present study, the effects of acute exposure to polyethylene microplastics with different particle sizes (20 µm [MPs-20] and 30 µm [MPs-30]) on metabolites in D. magna and the mechanisms of toxicity were investigated by combining metabolomics and traditional toxicology techniques. Exposure to both MPs-20 and MPs-30 resulted in significant accumulation of microplastics in the gut of D. magna and significantly reduced D. magna survival and heart rate. Metabolomics analysis revealed that MPs-20 and MPs-30 induced significant changes in up to 88 and 91 differential metabolites, respectively, and collectively induced significant changes in 75 metabolites in D. magna. Among lipid metabolites, MPs-20 specifically downregulated phosphatidylcholine and upregulated phosphatidylethanolamine, which mainly affected phospholipid metabolism, whereas MPs-30 specifically downregulated amino acid metabolites l-glutamine, l-glutamate and malic acid, which mainly interfered with energy metabolism. The results of this study provide novel insights into the mechanism of effects of microplastics on metabolic processes in D. magna.

Metabolic profiling of nanosilver toxicity in the gills of common carp.

Studies have shown silver nanoparticles (AgNPs) exposure can result in a series of toxic effects in fish gills. However, it is still unclear how AgNPs affect metabolite expression and their related molecular metabolic pathways in fish gills. In this study, we employed untargeted metabolomics to study the effects of AgNPs and silver supernatant ions on fish gill metabolites. The results showed that AgNPs can induce significant changes in 96 differentially expressed metabolites, which mainly affect amino acid metabolism and energy metabolism in fish gills. Among these metabolites, AgNPs specifically induce significant changes in 72 differentially expressed metabolites, including L-histidine, L-isoleucine, L-phenylalanine, and citric acid. These metabolites were significantly enriched in the pathways of aminoacyl-tRNA biosynthesis, ABC transporters, and the citrate cycle. In contrast, Ag+ supernatant exposure can specifically induce significant changes in 14 differentially expressed metabolites that mainly interfere with sphingolipid metabolism in fish gills. These specifically regulated fish gill metabolites include sphinganine, sphingosine, and phytosphingosine, which were significantly enriched in the sphingolipid metabolism pathway. Our results clearly reveal the effects and potential toxicity mechanisms of AgNPs on fish gill metabolites. Furthermore, our study further determined the unique functions of released silver ions in AgNPs toxicity in fish gills.

Integration of transcriptomics and metabolomics reveals damage and recovery mechanisms of fish gills in response to nanosilver exposure.

Toxic effects of silver nanoparticles (AgNPs) on fish gills have been widely reported but the recoverability of AgNPs-induced fish gill injuries is still unknown. In this study, combined multiomics and conventional toxicological analytical methods were used to investigate the changes in the gills of common carp responses to AgNPs (0.1 mg/L) toxicity after 24 h exposure and 7-day recovery. Conventional toxicological results showed that AgNPs exposure significantly increased silver content in gills and caused epithelial hyperplasia and lamellar fusion. After the recovery period, the silver content in fish gills significantly decreased; accompanied by the disappearance of histopathological characteristics in fish gills. Multiomics results revealed that AgNPs exposure resulted in the differential expression of 687 genes and 96 metabolites in fish gills. These differentially expressed genes (DEGs) and metabolites mainly participate in amino acid, carbohydrate, and lipid metabolisms, and are significantly enriched in the tricarboxylic acid (TCA) cycle. After the recovery period, the number of DEGs and metabolites in gills decreased to 33 and 90, respectively. Moreover, DEGs and metabolites in the TCA cycle recovered to control levels. In summary, the present study found that AgNPs-induced fish gill toxicity showed potential recoverability at molecular and phenotype levels.

Ecological risk assessment of heavy metals in fish from the Dianchi Lake, China using the integrated biomarker response approach.

This study used the integrated biomarker response (IBR) index approach to assess the ecological risks of heavy metals in different regions of Dianchi Lake, combined with active monitoring and passive monitoring. The contents of five heavy metals (Cu, As, Cd, Hg, and Pb) and six biomarkers (acetylcholinesterase, sodium-potassium ATPase, metallothionein, superoxide dismutase, glutathione peroxidase, and malondialdehyde) in the muscles of crucians (Carassius auratus) were measured to calculate the IBR value. The results indicate that the contents of heavy metal in the fish under active monitoring and passive monitoring were rather low and did not exceed the National Food Safety Standards of China. The IBR value of day 14 of active monitoring correlated with the heavy metal Cd content in the fish, suggesting a potential risk of Cd pollution in the aquatic environment of Dianchi Lake. The IBR values obtained for different regions of the lake on day 14 can be arranged in the following order: West S3 (9.24) > East S1 (3.97) > South S2 (2.39) > North S4 (0.36). These results suggest a potential risk of heavy metal contamination in the western part of Dianchi Lake.

Proteomic profiling reveals the differential toxic responses of gills of common carp exposed to nanosilver and silver nitrate.

Although the toxic effects of silver nanoparticles (AgNPs) on fish gills have been reported, the underlying mechanism of toxicity remains unclear. The present study aimed to elucidate the mechanism of toxicity in the gills of common carp following exposure to AgNPs and silver nitrate (AgNO3) using histopathology and proteomics. Histopathological findings revealed that both AgNPs and AgNO3 caused telangiectasia and epithelial cell hyperplasia in fish gills; however, the pathological features and location of lesions caused by the two forms of silver were markedly different. Proteomics revealed that AgNPs and AgNO3 induced 139 and 185 differential expression proteins (DEPs) in gills, respectively, and the two forms of silver induced only 42 shared proteins. AgNPs specifically induced 87 DEPs which mainly involved signaling mechanisms, cytoskeleton, and the arachidonic acid metabolism processes. AgNO3 specifically induced 125 DEPs that were mainly clustered in the glutathione metabolism and protease processes. These results suggested that the toxic effects of AgNPs and AgNO3 were dramatically different in terms of protein expression in fish gills, which may provide novel perspectives for understanding the toxicity mechanism of silver nanoparticles in fish gills.

Effect of silver nanoparticles on gill membranes of common carp: Modification of fatty acid profile, lipid peroxidation and membrane fluidity.

Although the toxicity of silver nanoparticles (AgNPs) in aquatic organisms has been extensively investigated, the mechanism by which AgNPs damage membranes remains unclear. This study investigated the toxic effects of a series of sub-lethal concentrations of AgNPs on the membranes of freshwater carp (Cyprinus carpio) gills, based on changes in membrane fatty acid (FA) profile, membrane fluidity, membrane lipid peroxidation, and histopathology. Most of the FAs in fish gill membrane was not significantly affected by exposure to multiple AgNPs concentrations, only few significant changes occurred in some specific FAs species at a high concentration of AgNPs exposure. In particular, high concentrations of AgNPs significantly decreased the proportions of two important long-chain n-3 series polyunsaturated FAs (C20: 5n3, and C22: 6n3), resulting in a decreased ratio of n-3 polyunsaturated FAs to n-6 polyunsaturated FAs (Σn-3UFA/Σn-6UFA). The AgNPs also caused a dose-dependent decrease in fish gill membrane fluidity, increased the level of lipid peroxidation, and inhibited Na+/K+-ATPase enzyme activity. Further histopathological examination revealed that exposure to AgNPs can cause toxic responses in the lamellae, including the thinning of the basement membrane, malformation, and inflammation. Together, the results suggest that the mechanism of AgNPs membrane toxicity involves the oxidization of long-chain omega-3 unsaturated FAs to saturated FAs via lipid peroxidation, resulting in, decreased membrane fluidity and ultimately the destruction of the normal physiological function of the fish gill membrane. The findings contribute significantly to our understanding of nanoparticle-induced membrane toxicity and potential risks in aquatic environments.