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1.
Ecotoxicol Environ Saf ; 203: 111001, 2020 Oct 15.
Artigo em Inglês | MEDLINE | ID: mdl-32888585

RESUMO

Environmental nanomaterials contamination is a great concern for organisms including human. Copper oxide nanoparticles (CuO NPs) are widely used in a huge range of applications which might pose potential risk to organisms. This study investigated the in vivo transgenerational toxicity on development and reproduction with parental CuO NPs exposure in the nematode Caenorhabditis elegans. The results showed that CuO NPs (150 mg/L) significantly reduced the body length of parental C. elegans (P0). Only about 1 mg/L Cu2+ (~0.73%) were detected from 150 mg/L CuO NPs in 0.5X K-medium after 48 h. In transgenerational assays, CuO NPs (150 mg/L) parental exposure significantly induced developmental and reproductive toxicity in non-exposed C. elegans progeny (CuO NPs free) on body length (F1) and brood size (F1 and F2), respectively. In contrast, parental exposure to Cu2+ (1 mg/L) did not cause transgenerational toxicity on growth and reproduction. This suggests that the transgenerational toxicity was mostly attributed to the particulate form of CuO NPs. Moreover, qRT-PCR results showed that the mRNA levels of met-2 and spr-5 genes were significantly decreased at P0 and F1 upon only maternal exposure to CuO NPs (150 mg/L), suggesting the observed transgenerational toxicity was associated with possible epigenetic regulation in C. elegans.


Assuntos
Caenorhabditis elegans/efeitos dos fármacos , Cobre/toxicidade , Epigênese Genética/efeitos dos fármacos , Nanopartículas/toxicidade , Animais , Caenorhabditis elegans/genética , Caenorhabditis elegans/crescimento & desenvolvimento , Caenorhabditis elegans/fisiologia , Feminino , Humanos , Exposição Materna/efeitos adversos , Reprodução/efeitos dos fármacos , Reprodução/genética
2.
Ecotoxicol Environ Saf ; 203: 111054, 2020 Oct 15.
Artigo em Inglês | MEDLINE | ID: mdl-32888616

RESUMO

Quinclorac (3,7-dichloroquinoline-8-carboxylic acid, QNC) is a highly selective auxin herbicide that is typically applied to paddy rice fields. Its residue is a serious problem in crop rotations. In this study, Oryza sativa L. seedlings was used as a model plant to explore its biochemical response to abiotic stress caused by QNC and nZVI coexposure, as well as the interactions between QNC and nZVI treatments. Exposure to 5 and 10 mg/L QNC reduced the fresh biomass by 26.6% and 33.9%, respectively, compared to the control. The presence of 50 and 250 mg/L nZVI alleviated the QNC toxicity, but the nZVI toxicity was aggravated by the coexist of QNC. Root length was enhanced upon exposure to low or medium doses of both QNC and nZVI, whereas root length was inhibited under high-dose coexposure. Both nZVI and QNC, either alone or in combination, significantly inhibited the biosynthesis of chlorophyll, and the inhibition rate increased with elevated nZVI and QNC concentration. It was indicated that nZVI or QNC can affect the plant photosynthesis, and there was a significant interaction between the two treatments. Effects of QNC on the antioxidant response of Oryza sativa L. differed in the shoots and roots; generally, the introduction of 50 and 250 mg/L nZVI alleviated the oxidative stress (POD in shoots, SOD and MDA in roots) induced by QNC. However, 750 mg/kg nZVI seriously damaged Oryza sativa L. seedlings, which likely resulted from active iron deficiency. QNC could be removed from the culture solution by nZVI; as a result, nZVI suppressed QNC uptake by 20%-30%.


Assuntos
Antioxidantes/metabolismo , Ferro/toxicidade , Nanopartículas/toxicidade , Oryza/efeitos dos fármacos , Estresse Oxidativo/efeitos dos fármacos , Quinolinas/toxicidade , Poluentes do Solo/toxicidade , Transporte Biológico , Biomassa , Clorofila/metabolismo , Relação Dose-Resposta a Droga , Interações Medicamentosas , Oryza/crescimento & desenvolvimento , Oryza/metabolismo , Raízes de Plantas/efeitos dos fármacos , Raízes de Plantas/crescimento & desenvolvimento , Raízes de Plantas/metabolismo , Plântula/efeitos dos fármacos , Plântula/crescimento & desenvolvimento , Plântula/metabolismo
3.
Chemosphere ; 254: 126608, 2020 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-32957262

RESUMO

Al2O3 Nanoparticles (Al2O3-NPs) have been widely used because of their unique physical and chemical properties, and Al2O3-NPs can be released into the environment directly or indirectly. Our previous research found that 13 nm Al2O3-NPs can induce neural cell death and autophagy in primarily cultured neural cells in vitro. The aim of this study was to determine where Al2O3-NPs at 13 nm particle size can cause neural cells in vivo and assess related behavioural changes and involved potential mechanisms. Zebrafish from embryo to adult were selected as animal models. Learning and memory as functional indicators of neural cells in zebrafish were measured during the development from embryo to adult. Our results indicate that Al2O3-NPs treatment in zebrafish embryos stages can cause the accumulation of aluminium content in zebrafish brain tissue, leading to progressive impaired neurodevelopmental behaviours and latent learning and memory performance. Additionally, oxidative stress and disruption of dopaminergic transmission in zebrafish brain tissues are correlated with the dose-dependent and age-dependent accumulation of aluminium content. Moreover, the number of neural cells in the telencephalon tissue treated with Al2O3-NPs significantly declined, and the ultramicroscopic morphology indicated profound autophagy alternations. The results suggest that Al2O3-NPs has dose-dependent and time-dependent progressive damage on learning and memory performance in adult zebrafish when treated in embryos. This is the first study of the effects of Al2O3-NPs on learning and memory during the development of zebrafish from embryo to adult.


Assuntos
Óxido de Alumínio/toxicidade , Aprendizagem/efeitos dos fármacos , Memória/efeitos dos fármacos , Nanopartículas/toxicidade , Alumínio/farmacologia , Óxido de Alumínio/química , Animais , Embrião não Mamífero , Nanopartículas Metálicas , Estresse Oxidativo/efeitos dos fármacos , Tamanho da Partícula , Peixe-Zebra/embriologia
4.
Chemosphere ; 254: 126792, 2020 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-32957266

RESUMO

Iron oxide nanoparticles (IONPs) are used in several medical and environmental applications, but their mechanism of action and hazardous effects to early developmental stages of fish remain unknown. Thus, the present study aimed to assess the developmental toxicity of citrate-functionalized IONPs (γ-Fe2O3 NPs), in comparison with its dissolved counterpart, in zebrafish (Danio rerio) after static and semi-static exposure. Embryos were exposed to environmental concentrations of both iron forms (0.3, 0.6, 1.25, 2.5, 5 and 10 mg L-1) during 144 h, jointly with negative control group. The interaction and distribution of both Fe forms on the external chorion and larvae surface were measured, following by multiple biomarker assessment (mortality, hatching rate, neurotoxicity, cardiotoxicity, morphological alterations and 12 morphometrics parameters). Results showed that IONPs were mainly accumulated on the zebrafish chorion, and in the digestive system and liver of the larvae. Although the IONPs induced low embryotoxicity compared to iron ions in both exposure conditions, these nanomaterials induced sublethal effects, mainly cardiotoxic effects (reduced heartbeat, blood accumulation in the heart and pericardial edema). The semi-static exposure to both iron forms induced high embryotoxicity compared to static exposure, indicating that the nanotoxicity to early developmental stages of fish depends on the exposure system. This is the first study concerning the role of the exposure condition on the developmental toxicity of IONPs on fish species.


Assuntos
Compostos Férricos/toxicidade , Poluentes Químicos da Água/toxicidade , Animais , Cloretos , Embrião não Mamífero/efeitos dos fármacos , Ferro/farmacologia , Larva/efeitos dos fármacos , Nanopartículas/toxicidade , Peixe-Zebra/embriologia
5.
Chemosphere ; 254: 126794, 2020 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-32957267

RESUMO

Present study carried out pot experiments and evaluated effects of single and binary mixture of nanoparticles (exposed via sludge as soil conditioner) on spinach plant. Exposure of Ag2O nanoparticles (NPs) (1 and 10 mg/kg soil-sludge) did not show significant reduction in plant as compared to control. On the other hand, TiO2 NPs (exposed as single and in binary mixture) resulted in significant increase in root length (29% and 37%) and fresh weight (60% and 48%) at highest exposure concentration. Total chlorophyll content decreased for Ag2O and binary mixture (7% and 4%, respectively) and increased for TiO2 (5%) at 10 mg/kg soil-sludge. The toxic interaction between Ag2O and TiO2 NPs was additive at both exposure concentrations. Ag2O NPs had higher tendency of root surface adsorption than TiO2 NPs. Metal content in spinach leaves at highest exposure concentration was Ag: 2.6 ± 0.55 mg/g plant biomass(for Ag2O NPs) and 1.02 ± 0.32 mg/g plant biomass (for Ag2O + TiO2 NPs) and for Ti: 1.12 ± 0.78 (for TiO2 NPs) mg/g plant biomass and 0.58 ± 0.41 mg/g (for Ag2O + TiO2 NPs). The inadvertent ingestion of NPs- contaminated spinach resulted in projected daily intake (DI) of Ag and Ti for different age-mass classes (child to adult) exceeding the oral reference dose for toxicity during oral ingestion. In conclusion, we report no acute toxicity of single and binary mixture of NPs to spinach but significant accumulation of Ag and Ti metals in spinach leaves. There are high chances that ingestion of spinach grown in such environment might lead to human health risks.


Assuntos
Nanopartículas/toxicidade , Poluentes do Solo/toxicidade , Spinacia oleracea/efeitos dos fármacos , Biomassa , Clorofila , Humanos , Nanopartículas Metálicas/toxicidade , Metais/toxicidade , Nanopartículas/análise , Folhas de Planta/química , Esgotos , Solo , Poluentes do Solo/análise , Spinacia oleracea/crescimento & desenvolvimento , Titânio/farmacologia
6.
Ecotoxicol Environ Saf ; 202: 110911, 2020 Oct 01.
Artigo em Inglês | MEDLINE | ID: mdl-32800246

RESUMO

Applications of TiO2 nanoparticles (NPs) in food, personal care products and industries pose risks on human health, particularly on vulnerable populations including pregnant women and infants. Fetus, deficient in mature defense system, is more susceptible to NPs. Publications on the developmental toxicity of TiO2 NPs on the maternal-exposed progeny have emerged. This review presents the main exposure routes of TiO2 NPs during pregnancy, including skin penetration, ingestion and inhalation, followed by transport of TiO2 NPs to the placenta. Accumulation of TiO2 NPs in placenta may cause dysfunction in nutrient transfer. TiO2 NPs can be even transported to the fetus and generate toxicities, such as impairments of nervous and reproductive system, and failure in lung and cardiovascular development. The toxicities rely on the crystalline phase and concentrations, and the main mechanisms include the accumulation of excessive reactive oxygen species, DNA damage, and over-activation of signaling pathways such as MAPK which impairs neurotransmission. Finally, this review remarks on the significance for identifying TiO2 NPs dosage safe for both mother and fetus, and particular attention should be paid at TiO2 NPs concentrations safe for mother but toxic to fetus. Importantly, research on the epigenetic trans-generational inheritance of TiO2 NPs is urgently needed to provide insights for deciding the prospects of TiO2 NPs applications.


Assuntos
Nanopartículas Metálicas/toxicidade , Titânio/toxicidade , Animais , Feminino , Feto , Humanos , Nanopartículas/toxicidade , Organogênese , Placenta/metabolismo , Gravidez , Efeitos Tardios da Exposição Pré-Natal/metabolismo , Espécies Reativas de Oxigênio/metabolismo , Testes de Toxicidade
7.
Ecotoxicol Environ Saf ; 203: 111032, 2020 Oct 15.
Artigo em Inglês | MEDLINE | ID: mdl-32745774

RESUMO

Titanium dioxide nanoparticles (Np-TiO2) have become the common component of sunscreen cosmetic products. Np-TiO2 can affect especially aquatic ecosystems health, including aquatic organisms such as fish. It is therefore necessary to acquire a better understanding of the effect of Np-TiO2 on aquatic organisms. This study evaluated the biological effects of Np-TiO2 on Danio rerio, such as survival rate and weight change and, in particular, the Ti content or retention in the intestine and liver, as well as the activities of catalase and superoxide dismutase enzymes. In addition, the structure of the intestine, kidney, and liver was investigated through histological analysis. Ninety zebrafish were used, randomly divided into three treatment-groups: a control group (fed with food without adding Np-TiO2) and two groups of fish fed with food containing Np-TiO2 exposed for 7 and 14 days. The amount of Ti in the liver and intestine was measured using atomic absorption spectrophotometry coupled to a graphite furnace (GFAAS). Morphological analysis and enzyme catalase and superoxide dismutase assays were likewise performed. Ti was detected in all fish even in control group; probably Ti must have been introduced during production by the fish food industry. Structural changes were detected in fish fed with Np-TiO2 as vacuolization and disruption of the apical cytoplasm of epithelial cells that covered the intestinal villi. Although kidney morphology appeared intact, the lumen of the proximal tubule was enlarged, and the cells of the distal tubule were vacuolated. No morphological changes in the liver were detected; however, superoxide dismutase activity decreased, suggesting that liver changes occurred at the molecular level. Thus, Np-TiO2 causes morphological changes in the intestine, kidney, and liver of zebrafish and biochemical changes in the liver exposed for 7 and 14 days. Although not highly lethal, Np-TiO2 in the food chain can interfere with the morphophysiology of aquatic organisms. Neither mortalities nor body weight losses were recorded among fish in all groups over the duration of the experiment.


Assuntos
Mucosa Intestinal/efeitos dos fármacos , Rim/efeitos dos fármacos , Fígado/efeitos dos fármacos , Nanopartículas/toxicidade , Titânio/toxicidade , Poluentes Químicos da Água/toxicidade , Peixe-Zebra , Animais , Bioacumulação , Catalase , Relação Dose-Resposta a Droga , Ecossistema , Cadeia Alimentar , Mucosa Intestinal/metabolismo , Mucosa Intestinal/patologia , Rim/metabolismo , Rim/patologia , Fígado/metabolismo , Fígado/patologia , Nanopartículas/metabolismo , Distribuição Aleatória , Protetores Solares/química , Titânio/metabolismo , Poluentes Químicos da Água/metabolismo
8.
Ecotoxicol Environ Saf ; 202: 110960, 2020 Oct 01.
Artigo em Inglês | MEDLINE | ID: mdl-32800232

RESUMO

Zinc oxide nanoparticles (ZnO NPs) have been extensively used in various industries and reported to inhibit spermatogenesis, however, ZnO NPs-induced spermatogenesis failure is yet to be fully elucidated. Herein, mouse-derived spermatogonia cell line GC-1 spg cells were treated with ZnO NPs for 24 h in the presence or absence of radical scavenger N-acetyl-L-cysteine (NAC) or autophagy inhibitor 3-methyladenine (3-MA), then cell viability was observed by MTT assay; apoptosis was observed by western blotting analysis and AnnexinV-FITC/PI assay, respectively; autophagy was detected by western blotting analysis and transmission electron microscopy, respectively; and the contents of MDA and GSH and the activities of SOD and GSH-PX were measured by oxidative stress kits. The present study showed that ZnO NPs exposure inhibited viability and induced apoptosis of mouse GC-1 spg cells. Intriguingly, ZnO NPs markedly increased the protein content of LC3-II, the ratio of LC3-II/LC3-I, and the protein levels of ATG 5 and Beclin 1 in the cells. Furthermore, transmission electron microscopy (TEM) showed that autophagic vesicles in the cytoplasm increased significantly in the ZnO NPs-treated cells, indicating that ZnO NPs could induce autophagy of the cells. Oxidative stress could be induced by ZnO NPs; moreover, inhibition of oxidative stress could alleviate the induction of apoptosis and autophagy by ZnO NPs. Inhibition of autophagy by 3-MA could rescue the inhibition of cell viability and induction of apoptosis by ZnO NPs, which indicated that autophagy might have cytotoxic effect on ZnO NPs-induced apoptosis. In summary, oxidative stress was involved in ZnO NPs-induced apoptosis and autophagy of mouse GC-1 spg cells, and autophagy might play a cytotoxic role in ZnO NPs-induced apoptosis.


Assuntos
Apoptose/efeitos dos fármacos , Autofagia/efeitos dos fármacos , Nanopartículas/toxicidade , Estresse Oxidativo/efeitos dos fármacos , Óxido de Zinco/toxicidade , Animais , Proteína Beclina-1/metabolismo , Linhagem Celular , Sobrevivência Celular/efeitos dos fármacos , Humanos , Camundongos , Microscopia Eletrônica de Transmissão , Espécies Reativas de Oxigênio/metabolismo , Espermatogênese/efeitos dos fármacos
9.
Sci Total Environ ; 745: 141055, 2020 Nov 25.
Artigo em Inglês | MEDLINE | ID: mdl-32736110

RESUMO

Plant seedlings are susceptible to copper (Cu) toxicity. As copper levels in soil continue to rise with the use of Cu-based agrochemicals, alleviation of Cu stress is of paramount importance. Traditional approaches to allay Cu stress are well documented but are typically found to be either costly or inefficient. Given their small size, ionic character, and high biocompatibility, specific polymeric nanoparticles (NPs) may have the potential for mitigating metal toxicity to crops. In this pioneering study, we investigated the effects of newly synthesized polysuccinimide NPs (PSI-NPs) on corn (Zea mays L.) seed germination and seedling growth under different levels of Cu stress. The results showed that PSI-NPs influenced seed germination in a dose-dependent manner with an optimal rate of 200 mg L-1. In addition, the positive effects of PSI-NPs on seed germination indexes were found to be positively correlated with enhanced seed imbibition (r = 0.82). The addition of PSI-NPs significantly mitigated Cu stress as indicated by improved growth of shoots and roots, and higher antioxidant enzyme activity observed with co-exposure to PSI-NPs as compared to Cu stress treatment only. Cu concentrations in seedling root and shoot significantly increased with increasing Cu treatment rate. Higher uptake of Cu by plant was observed in the Cu-PSI-NPs co-treatment than single Cu treatment. The alleviation effect of PSI-NPs could be explained by the enhanced antioxidant enzyme activities and storage of Cu as Cu-PSI complexes in plants with reduced phytotoxicity. These findings will open the opportunity of using PSI-NPs as a regulator to enhance seed germination and improve seedling growth under stress of heavy metals like Cu.


Assuntos
Germinação , Nanopartículas/toxicidade , Cobre/toxicidade , Raízes de Plantas , Plântula , Sementes
10.
Int J Nanomedicine ; 15: 5227-5237, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32801688

RESUMO

Background: Large-scale production and application of amorphous silica nanoparticles (SiNPs) have enhanced the risk of human exposure to SiNPs. However, the toxic effects and the underlying biological mechanisms of SiNPs on Caenorhabditis elegans remain largely unclear. Purpose: This study was to investigate the genome-wide transcriptional alteration of SiNPs on C. elegans. Methods and Results: In this study, a total number of 3105 differentially expressed genes were identified in C. elegans. Among them, 1398 genes were significantly upregulated and 1707 genes were notably downregulated in C. elegans. Gene ontology analysis revealed that the significant change of gene functional categories triggered by SiNPs was focused on locomotion, determination of adult lifespan, reproduction, body morphogenesis, multicellular organism development, endoplasmic reticulum unfolded protein response, oocyte development, and nematode larval development. Meanwhile, we explored the regulated effects between microRNA and genes or signaling pathways. Pathway enrichment analysis and miRNA-gene-pathway-network displayed that 23 differential expression microRNA including cel-miR-85-3p, cel-miR-793, cel-miR-241-5p, and cel-miR-5549-5p could regulate the longevity-related pathways and inflammation signaling pathways, etc. Additionally, our data confirmed that SiNPs could disrupt the locomotion behavior and reduce the longevity by activating ins-7, daf-16, ftt-2, fat-5, and rho-1 genes in C. elegans. Conclusion: Our study showed that SiNPs induced the change of the whole transcriptome in C. elegans, and triggered negative effects on longevity, development, reproduction, and body morphogenesis. These data provide abundant clues to understand the molecular mechanisms of SiNPs in C. elegans.


Assuntos
Caenorhabditis elegans/efeitos dos fármacos , Caenorhabditis elegans/genética , Regulação da Expressão Gênica/efeitos dos fármacos , Nanopartículas/toxicidade , Animais , Proteínas de Caenorhabditis elegans/genética , Redes Reguladoras de Genes/efeitos dos fármacos , Genoma Helmíntico , Humanos , Longevidade/efeitos dos fármacos , MicroRNAs/genética , Testes de Mutagenicidade/métodos , Nanopartículas/química , Reprodução/efeitos dos fármacos , Transdução de Sinais/efeitos dos fármacos , Dióxido de Silício/química , Dióxido de Silício/toxicidade , Transcriptoma , Resposta a Proteínas não Dobradas/genética
11.
Int J Nanomedicine ; 15: 4393-4405, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32606684

RESUMO

Aim: The effects of polyamidoamine (PAMAM) dendrimers on the mammalian heart are not completely understood. In this study, we have investigated the effects of a sixth-generation cationic dendrimer (G6 PAMAM) on cardiac function in control and diabetic rat hearts following ischemia-reperfusion (I/R) injury. Methods: Isolated hearts from healthy non-diabetic (Ctr) male Wistar rats were subjected to ischemia and reperfusion (I/R). LV contractility and hemodynamics data were computed digitally whereas cardiac damage following I/R injury was assessed by measuring cardiac enzymes. For ex vivo acute exposure experiments, G6 PAMAM was administered during the first 10 mins of reperfusion in Ctr animals. In chronic in vivo studies, nondiabetic rats (Ctr) received either vehicle or daily i.p. injections of G6 PAMAM (40 mg/kg) for 4 weeks. Diabetic (D) animals received either vehicle or daily i.p. injections of G6 PAMAM (10, 20 or 40 mg/kg) for 4 weeks. The impact of G6 PAMAM on pacing-postconditioning (PPC) was also studied in Ctr and D rats. Results: In ex vivo studies, acute administration of G6 PAMAM to isolated Ctr hearts during reperfusion dose-dependently impaired recovery of cardiac hemodynamics and vascular dynamics parameters following I/R injury. Chronic daily i.p. injections of G6 PAMAM significantly (P<0.01) impaired recovery of cardiac function following I/R injury in nondiabetic animals but this was not generally observed in diabetic animals except for CF which was impaired by about 50%. G6 PAMAM treatment completely blocked the protective effects of PPC in the Ctr animals. Conclusion: Acute ex vivo or chronic in vivo treatment with naked G6 PAMAM dendrimer can significantly compromise recovery of non-diabetic hearts from I/R injury and can further negate the beneficial effects of PPC. Our findings are therefore extremely important in the nanotoxicological evaluation of G6 PAMAM dendrimers for potential clinical applications in physiological and pathological settings.


Assuntos
Dendrímeros/toxicidade , Coração/fisiopatologia , Mamíferos/fisiologia , Traumatismo por Reperfusão Miocárdica/fisiopatologia , Nanopartículas/toxicidade , Poliaminas/administração & dosagem , Recuperação de Função Fisiológica/efeitos dos fármacos , Animais , Diabetes Mellitus Experimental/patologia , Diabetes Mellitus Experimental/fisiopatologia , Coração/efeitos dos fármacos , Hemodinâmica/efeitos dos fármacos , Pós-Condicionamento Isquêmico , Masculino , Contração Miocárdica/efeitos dos fármacos , Miocárdio/enzimologia , Ratos Wistar
12.
Int J Nanomedicine ; 15: 4407-4415, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32606685

RESUMO

Objective: Silica nanoparticles (SiO2 NPs) have been extensively employed in biomedical field. SiO2 NPs are primarily designed to enter the circulatory system; however, little information is available on potential adverse effects of SiO2 NPs on the nervous system. Methods: The neurotoxicity of SiO2 NPs at different concentrations (3, 6, 12 ng/nL) on zebrafish embryos was determined using immunofluorescence and microarray techniques, and subsequently confirmed by qRT-PCR. Results: SiO2 NPs disrupt the axonal integrity and decrease the length of axons in Tg (NBT: EGFP) transgenic lines. The number of apoptotic cells in the brain and central nervous system of zebrafish embryos was increased in the presence of 12 ng/nL of SiO2 NPs, but the difference did not reach statistical significance. Screening for changes in the expression of genes involved in the neuroactive ligand-receptor interaction pathway was performed by microarray and confirmed by qRT-PCR. These analyses demonstrated that SiO2 NPs markedly downregulated genes associated with neural function (grm6a, drd1b, chrnb3b, adrb2a, grin2ab, npffr2.1, npy8br, gabrd, chrma3, gabrg3, gria3a, grm1a, adra2b, and glra3). Conclusion: The obtained results documented that SiO2 NPs can induce developmental neurotoxicity by affecting the neuroactive ligand-receptor interaction signaling pathway. This new evidence may help to clarify the mechanism of SiO2 NPs-mediated neurotoxicity.


Assuntos
Embrião não Mamífero/metabolismo , Nanopartículas/toxicidade , Neurotoxinas/toxicidade , Receptores de Superfície Celular/metabolismo , Transdução de Sinais , Dióxido de Silício/toxicidade , Peixe-Zebra/embriologia , Animais , Apoptose/efeitos dos fármacos , Embrião não Mamífero/efeitos dos fármacos , Ligantes , Transdução de Sinais/efeitos dos fármacos
13.
PLoS One ; 15(7): e0232745, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32609722

RESUMO

Microplastics or plastic particles less than 5 mm in size are a ubiquitous and damaging pollutant in the marine environment. However, the interactions between these plastic particles and marine microorganisms are just starting to be understood. The objective of this study was to measure the responses of a characteristic marine organism (Synechococcus sp. PCC 7002) to an anthropogenic stressor (polyethelene nanoparticles and microparticles) using molecular techniques. This investigation showed that polyethylene microparticles and nanoparticles have genetic, enzymatic and morphological effects on Synechococcus sp. PCC 7002. An RT-PCR analysis showed increases in the expression of esterase and hydrolase genes at 5 days of exposure to polyethylene nanoparticles and at 10 days of exposure to polyethylene microparticles. A qualitative enzymatic assay also showed esterase activity in nanoparticle exposed samples. Cryo-scanning electron microscopy was used to assess morphological changes in exopolymer formation resulting from exposure to polyethylene microparticles and nanoparticles. The data from this paper suggests that microplastic and nanoplastics could be key microbial stressors and should be investigated in further detail.


Assuntos
Microplásticos/toxicidade , Nanopartículas/toxicidade , Polietileno/química , Polietileno/toxicidade , Estresse Fisiológico/efeitos dos fármacos , Synechococcus/efeitos dos fármacos , Synechococcus/fisiologia , Biofilmes/efeitos dos fármacos , Atividades Humanas , Microplásticos/química , Nanopartículas/química , Tamanho da Partícula , Synechococcus/citologia , Synechococcus/genética , Poluentes Químicos da Água/química , Poluentes Químicos da Água/toxicidade
14.
PLoS One ; 15(7): e0235556, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32614916

RESUMO

To gain a better insight into the selenium nanoparticle (nSe) benefits/toxicity, this experiment was carried out to address the behavior of bitter melon seedlings to nSe (0, 1, 4, 10, 30, and 50 mgL-1) or bulk form (selenate). Low doses of nSe increased biomass accumulation, while concentrations of 10 mgL-1 and above were associated with stem bending, impaired root meristem, and severe toxicity. Responses to nSe were distinct from that of bulk in that the nano-type exhibited a higher efficiency to stimulate growth and organogenesis than the bulk. The bulk form displayed higher phytotoxicity than the nano-type counterpart. According to the MSAP-based analysis, nSe mediated substantial variation in DNA cytosine methylation, reflecting the epigenetic modification. By increasing the concentration of nSe, the expression of the WRKY1 transcription factor linearly up-regulated (mean = 7.9-fold). Transcriptions of phenylalanine ammonia-lyase (PAL) and 4-Coumarate: CoA-ligase (4CL) genes were also induced. The nSe treatments at low concentrations enhanced the activity of leaf nitrate reductase (mean = 52%) in contrast with the treatment at toxic concentrations. The toxic concentration of nSe increased leaf proline concentration by 80%. The nSe supplement also stimulated the activities of peroxidase (mean = 35%) and catalase (mean = 10%) enzymes. The nSe-treated seedlings exhibited higher PAL activity (mean = 39%) and soluble phenols (mean = 50%). The nSe toxicity was associated with a disrupted differentiation of xylem conducting tissue. The callus formation and performance of the explants originated from the nSe-treated seedlings had a different trend than that of the control. This experiment provides new insights into the nSe-associated advantage/ cytotoxicity and further highlights the necessity of designing convincing studies to introduce novel methods for plant cell/tissue cultures and agriculture.


Assuntos
Metilação de DNA/efeitos dos fármacos , Epigênese Genética/efeitos dos fármacos , Momordica charantia/metabolismo , Nanopartículas/toxicidade , Selênio/química , Citosina/metabolismo , Momordica charantia/efeitos dos fármacos , Momordica charantia/crescimento & desenvolvimento , Nanopartículas/química , Nitrato Redutase/genética , Nitrato Redutase/metabolismo , Fenóis/metabolismo , Fenilalanina Amônia-Liase/genética , Fenilalanina Amônia-Liase/metabolismo , Folhas de Planta/enzimologia , Folhas de Planta/metabolismo , Proteínas de Plantas/genética , Proteínas de Plantas/metabolismo , Raízes de Plantas/anatomia & histologia , Raízes de Plantas/crescimento & desenvolvimento , Raízes de Plantas/metabolismo , Prolina/metabolismo , Fatores de Transcrição/genética , Fatores de Transcrição/metabolismo , Regulação para Cima/efeitos dos fármacos
15.
Nanotoxicology ; 14(7): 985-1007, 2020 09.
Artigo em Inglês | MEDLINE | ID: mdl-32619159

RESUMO

Recent studies reported adverse liver effects and intestinal tumor formation after oral exposure to titanium dioxide (TiO2). Other oral toxicological studies, however, observed no effects on liver and intestine, despite prolonged exposure and/or high doses. In the present assessment, we aimed to better understand whether TiO2 can induce such effects at conditions relevant for humans. Therefore, we focused not only on the clinical and histopathological observations, but also used Adverse Outcome Pathways (AOPs) to consider earlier steps (Key Events). In addition, aiming for a more accurate risk assessment, the available information on organ concentrations of Ti (resulting from exposure to TiO2) from oral animal studies was compared to recently reported concentrations found in human postmortem organs. The overview obtained with the AOP approach indicates that TiO2 can trigger a number of key events in liver and intestine: Reactive Oxygen Species (ROS) generation, induction of oxidative stress and inflammation. TiO2 seems to be able to exert these early effects in animal studies at Ti liver concentrations that are only a factor of 30 and 6 times higher than the median and highest liver concentration found in humans, respectively. This confirms earlier conclusions that adverse effects on the liver in humans as a result of (oral) TiO2 exposure cannot be excluded. Data for comparison with Ti levels in human intestinal tissue, spleen and kidney with effect concentrations were too limited to draw firm conclusions. The Ti levels, though, are similar or higher than those found in liver, suggesting these tissues may be relevant too.


Assuntos
Mucosa Intestinal/efeitos dos fármacos , Rim/efeitos dos fármacos , Fígado/efeitos dos fármacos , Nanopartículas/toxicidade , Baço/efeitos dos fármacos , Titânio/toxicidade , Administração Oral , Animais , Aditivos Alimentares/química , Aditivos Alimentares/metabolismo , Aditivos Alimentares/toxicidade , Humanos , Inflamação , Mucosa Intestinal/metabolismo , Mucosa Intestinal/patologia , Rim/metabolismo , Rim/patologia , Fígado/metabolismo , Fígado/patologia , Nanopartículas/química , Nanopartículas/metabolismo , Estresse Oxidativo/efeitos dos fármacos , Baço/metabolismo , Baço/patologia , Titânio/química , Titânio/metabolismo
16.
Ecotoxicol Environ Saf ; 203: 110951, 2020 Oct 15.
Artigo em Inglês | MEDLINE | ID: mdl-32678752

RESUMO

The growing use of rare-earth doped upconversion nanoparticles (UCNPs) has caused increasing concern about their biosafety. Here, to understand the toxicity of UCNPs and their mechanism in HepG2 cells, we systematically study the cytotoxicity, uptake and elimination behaviors of three types of UCNPs combined multiple cytotoxicity evaluation means with inductively coupled plasma mass spectrometry (ICP-MS) detection. Sodium yttrium fluoride, doped with 18% (molar ratio) ytterbium and 2% erbium (NaYF4: Yb3+, Er3+) was selected as the model UCNPs with two sizes (35 and 55 nm), and the poly(acrylic acid) and polyethylenimine were selected as the representatives of negative and positive surface coating of UCNPs, respectively. UCNPs were found to induce cytotoxicity in time- and dose-dependent manners, which might be mediated by reactive oxygen species generation and oxidative stress. Apoptosis, inflammation, and metabolic process were enhanced after cells exposed to 200 mg/L UCNPs for 48 h. Increase in the protein levels of cleaved caspased-9, cleaved caspase-3 and Bax and decrease in the anti-apoptotic protein, Bcl-2 suggested that the mitochondria mediated pathway was involved in UCNP-induced apoptosis. With the aid of ICP-MS, it demonstrated that the cytotoxicity was associated with internalized amount of UCNPs, which largely relied on their surface properties rather than size in the tested range. By comparing UCNPs with Y3+ ions, it demonstrated that NPs properties played a nonnegligible role in the cytotoxicity of UCNPs. These findings provide new insights for fundamental understanding of cytotoxicity of UCNPs and may contribute to more rational use of these materials in the future.


Assuntos
Endocitose/efeitos dos fármacos , Érbio/toxicidade , Fluoretos/toxicidade , Nanopartículas/toxicidade , Itérbio/toxicidade , Ítrio/toxicidade , Apoptose/efeitos dos fármacos , Técnicas de Cultura de Células , Sobrevivência Celular , Érbio/química , Érbio/metabolismo , Fluoretos/química , Fluoretos/metabolismo , Expressão Gênica/efeitos dos fármacos , Células Hep G2 , Humanos , Potencial da Membrana Mitocondrial/efeitos dos fármacos , Nanopartículas/química , Nanopartículas/metabolismo , Estresse Oxidativo/efeitos dos fármacos , Tamanho da Partícula , Propriedades de Superfície , Itérbio/química , Itérbio/metabolismo , Ítrio/química , Ítrio/metabolismo
17.
Int J Nanomedicine ; 15: 3415-3431, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32523341

RESUMO

Purpose: Lanthanum oxide (La2O3) nanoparticles (NPs) have been widely used in catalytic and photoelectric applications, but the reproductive toxicity is still unclear. This study evaluated the reproductive toxicity of two different-sized La2O3 particles in the testes. Materials and Methods: Fifty Kunming mice were randomly divided into five groups. Mice were treated with La2O3 NPs by repeated intragastric administration for 90 days (control, nano-sized with 5, 10, 50 mg/kg BW and micro-sized with 50 mg/kg BW). Mice in the control group were treated with de-ionised water without La2O3 NPs. Sperm parameters, testicular histopathology, TEM assessment, hormone assay and nuclear factor erythroid 2-related factor 2 (Nrf-2) pathway were performed and evaluated. Results: The body weight of mice treated with La2O3 NPs or not had no difference; sperm parameters and histological assessment showed that La2O3 NPs could induce reproductive toxicity in the testicle. Serum testosterone and gonadotropin-releasing hormone (GnRH) in the NH (nano-sized with 50 mg/kg BW) group were markedly decreased relative to control group, and an increase of luteinizing hormone (LH) in NH group was detected . Additionally, transmission electron microscopy revealed that the ultrastructural abnormalities induced by La2O3 NPs were more severe than La2O3 MPs in the testes. Furthermore, La2O3 NPs treatment inhibited the translocation of nuclear factor erythroid 2-related factor 2 (Nrf-2) from the cytoplasm into the nucleus as well as the expression of downstream genes NAD(P)H quinone oxidoreductase1 (NQO1), hemeoxygenase 1 (HO-1) and (glutathione peroxidase) GSH-Px, thus abrogating Nrf-2-mediated defense mechanisms against oxidative stress. Conclusions: The results of this study demonstrated that La2O3 NPs improved the spermatogenesis defects in mice. La2O3 NPs inhibited Nrf-2/ARE signaling pathway that resulted in apoptosis in the mice testes.


Assuntos
Elementos de Resposta Antioxidante/genética , Lantânio/toxicidade , Fator 2 Relacionado a NF-E2/metabolismo , Nanopartículas/toxicidade , Óxidos/toxicidade , Reprodução/efeitos dos fármacos , Transdução de Sinais , Animais , Apoptose/efeitos dos fármacos , Regulação da Expressão Gênica/efeitos dos fármacos , Concentração de Íons de Hidrogênio , Inflamação/patologia , Lantânio/sangue , Masculino , Camundongos , Nanopartículas/ultraestrutura , Estresse Oxidativo/efeitos dos fármacos , Óxidos/sangue , Transdução de Sinais/efeitos dos fármacos , Espermatozoides/efeitos dos fármacos , Espermatozoides/metabolismo , Testículo/efeitos dos fármacos , Testículo/metabolismo , Testículo/patologia , Testículo/ultraestrutura , Testosterona/biossíntese , Testosterona/metabolismo
18.
Int J Nanomedicine ; 15: 3291-3302, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32494130

RESUMO

Background: Inhaled nanoparticles can cross pulmonary air-blood barrier into circulation and cause vascular endothelial injury and progression of cardiovascular disease. However, the molecular mechanism underlying the vascular toxicity of copper oxide nanoparticles (CuONPs) remains unclear. We have recently demonstrated that the release of copper ions and the accumulation of superoxide anions contributed to CuONPs-induced cell death in human umbilical vein endothelial cells (HUVECs). Herein, we further demonstrate the mechanism underlying copper ions-induced cell death in HUVECs. Methods and Results: CuONPs were suspended in culture medium and vigorously vortexed for several seconds before exposure. After treatment with CuONPs, HUVECs were collected, and cell function assays were conducted to elucidate cellular processes including cell viability, oxidative stress, DNA damage and cell signaling pathways. We demonstrated that CuONPs uptake induced DNA damage in HUVECs as evidenced by γH2AX foci formation and increased phosphorylation levels of ATR, ATM, p53 and H2AX. Meanwhile, we showed that CuONPs exposure induced oxidative stress, indicated by the increase of cellular levels of superoxide anions, the upregulation of protein levels of heme oxygenase-1 (HO-1) and glutamate-cysteine ligase modifier subunit (GCLM), the elevation of the levels of malondialdehyde (MDA), but the reduction of glutathione to glutathione disulfide ratio. We also found that antioxidant N-acetyl-L-cysteine (NAC) could ameliorate CuONPs-induced oxidative stress and cell death. Interestingly, we demonstrated that p38 mitogen-activated protein kinase (MAPK) signaling pathway was activated in CuONPs-treated HUVECs, while p38α MAPK knockdown by siRNA significantly rescued HUVECs from CuONPs-induced DNA damage and cell death. Importantly, we showed that copper ions chelator tetrathiomolybdate (TTM) could alleviate CuONPs-induced oxidative stress, DNA damage, p38 MAPK pathway activation and cell death in HUVECs. Conclusion: We demonstrated that CuONPs induced oxidative DNA damage and cell death via copper ions-mediated p38 MAPK activation in HUVECs, suggesting that the release of copper ions was the upstream activator for CuONPs-induced vascular endothelial toxicity, and the copper ions chelator TTM can alleviate CuONPs-associated cardiovascular disease.


Assuntos
Cobre/toxicidade , Dano ao DNA , Células Endoteliais da Veia Umbilical Humana/efeitos dos fármacos , Células Endoteliais da Veia Umbilical Humana/patologia , Nanopartículas/toxicidade , Estresse Oxidativo/efeitos dos fármacos , Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo , Morte Celular/efeitos dos fármacos , Ativação Enzimática/efeitos dos fármacos , Células Endoteliais da Veia Umbilical Humana/metabolismo , Humanos , Modelos Biológicos , Molibdênio/química , Nanopartículas/ultraestrutura
19.
Mar Environ Res ; 158: 105005, 2020 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-32501269

RESUMO

In order to investigate the combined toxicities of copper nanoparticles (nano-Cu) with microplastic on microalgae Skeletonema costatum, growth inhibition tests were carried out. The toxic effects of copper nanoparticles and microplastic on the microalgae under singleness and coexistence conditions were investigated. Both copper nanoparticles and microplastic inhibited the growth of S. costatum. The growth inhibition ratio (IR) increased with the increasing of particle concentrations and incubation time. The toxicity of copper nanoparticles was reduced with the addition of microplastic. The concentrations of Cu2+ in the medium with or without addition of microplastic were determined. It was found that adsorption of Cu2+ on microplastic and aggregation between copper nanoparticles and microplastic are the main reasons for attenuation of toxicity of nano-Cu with adding microplastic. The adhesion and aggregate interactions between microalgae and nanomaterial were also approved by the observations through scanning electron microscopy.


Assuntos
Cobre , Diatomáceas , Microalgas , Nanopartículas , Cobre/toxicidade , Microalgas/efeitos dos fármacos , Microalgas/crescimento & desenvolvimento , Microplásticos , Nanopartículas/toxicidade , Plásticos
20.
Ecotoxicol Environ Saf ; 201: 110857, 2020 Sep 15.
Artigo em Inglês | MEDLINE | ID: mdl-32534332

RESUMO

Caenorhabditis elegans is sensitive to toxicity of environmental pollutants. The alteration in expression of mir-794, a microRNA (miRNA) molecule, mediated a protective response to nanopolystyene (100 nm) at predicted environmental concentration (1 µg/L) in nematodes. However, the underlying molecular basis for mir-794 function in regulating the response to nanopolystyrene remains largely unclear. In this study, we found that intestinal overexpression of mir-794 caused the susceptibility to nanopolystyrene toxicity, suggesting that mir-794 acted in the intestine to regulate the response to nanopolystyrene. Intestinal overexpression of mir-794 further decreased the expressions of daf-16 encoding a FOXO transcriptional factor in insulin signaling pathway, skn-1 encoding a Nrf transcriptional factor in p38 MAPK signaling pathway, and mdt-15 encoding a lipid metabolic sensor acting downstream of SKN-1 in nanopolystyrene exposed nematodes. Meanwhile, intestinal overexpression of mir-794 could suppress the resistance of nematodes overexpressing intestinal daf-16, skn-1, or mdt-15 containing the corresponding 3' untranslated region (3' UTR) to nanopolystyrene toxicity. Therefore, DAF-16, SKN-1, and MDT-15 acted as the downstream targets of intestinal mir-794 to regulate the response to nanopolystyrene. In the intestine, DAF-16 functioned synergistically with SKN-1 or MDT-15 to regulate the response to nanopolystyrene. Our results suggested that the intestinal mir-794 provided an important epigenetic regulation mechanism to control the response to nanopolystyrene by linking insulin and p38 MAPK signaling pathways in nematodes.


Assuntos
Caenorhabditis elegans/efeitos dos fármacos , Insulina/metabolismo , Intestinos/efeitos dos fármacos , MicroRNAs/metabolismo , Nanopartículas/toxicidade , Poliestirenos/toxicidade , Poluentes do Solo/toxicidade , Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo , Animais , Caenorhabditis elegans/genética , Caenorhabditis elegans/metabolismo , Proteínas de Caenorhabditis elegans/genética , Proteínas de Caenorhabditis elegans/metabolismo , Epigênese Genética , Regulação da Expressão Gênica , Lipídeos , Sistema de Sinalização das MAP Quinases/efeitos dos fármacos , MicroRNAs/genética , Fatores de Transcrição/genética
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