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1.
Ecotoxicol Environ Saf ; 208: 111685, 2021 Jan 15.
Artigo em Inglês | MEDLINE | ID: mdl-33396017

RESUMO

The wastewater utilization for irrigation purposes is common practice in peri-urban areas located in vicinity of developed cities. This water contains elements like chromium (Cr), nickel (Ni), cadmium (Cd) and nitrate (NO3-N) that poses health risk when exposed to human. In this study effect of wastewater irrigation from Chakara wastewater plant, Faisalabad on growth of wheat and health risks was assessed. Pot experiment was conducted at Institute of Soil and Environmental, University of Agriculture, Faisalabad using different concentration of wastewater as treatment 100% tap water, 25% wastewater + 75% tap water, 50% wastewater + 50% tap water, 75% wastewater + 25% tap water, 100% wastewater. The results indicated that the wastewater irrigation negatively effects the plant growth and physiological parameters. The minimum plant height, grain weight, spike length, osmotic potential and SPAD values were recorded 50.33 cm, 1.47 g plant-1, 7.00 cm, 423 and 38.91 respectively in 100% wastewater irrigation. The risk quotient (RQ TEs) for each toxic element and cumulative risk index (RI TEs) values were calculated. The cadmium risk quotient (Cd RQ) for adults was on margin and value was >1 for in 75% wastewater + 25% tap water and 100% wastewater irrigation, while the RQ for Ni and Cr was <1. Maximum RI TEs values calculated in 100% wastewater irrigation 0.424 and 0.294 for children and adults respectively. Hence it was concluded that wastewater irrigation significantly increased the accumulation rate of metals and nitrate in wheat and cause potential health risks for children and adults.


Assuntos
Irrigação Agrícola/métodos , Bioacumulação/efeitos dos fármacos , Metais Pesados/toxicidade , Nitratos/toxicidade , Poluentes do Solo/toxicidade , Triticum/efeitos dos fármacos , Águas Residuárias/química , Adulto , Cádmio/análise , Cádmio/toxicidade , Criança , Cromo/análise , Cromo/toxicidade , Cidades , Grão Comestível/química , Humanos , Metais Pesados/análise , Modelos Teóricos , Níquel/análise , Níquel/toxicidade , Nitratos/análise , Paquistão , Medição de Risco , Solo/química , Poluentes do Solo/análise , Triticum/crescimento & desenvolvimento , Triticum/metabolismo , Águas Residuárias/análise
2.
Sci Total Environ ; 753: 141743, 2021 Jan 20.
Artigo em Inglês | MEDLINE | ID: mdl-32891989

RESUMO

Nickel oxide nanoparticles (NiO-NPs) have extensively used in industrial and consumer products. The present study conducted to gain more knowledge about the safe use of NiO-NPs and also to understand their impact on the environment and biological systems. Herein, we examined the genotoxic and ultra-structural effects of a sublethal dose of NiO-NPs (0.03 mg/g) on the ovarian tissues of the ground beetle, Blaps polycresta. The mean diameter of NiO-NPs was 24.49 ± 3.88 nm, as obtained through transmission electron microscopy (TEM). In terms of DNA damage levels, the frequency of micronucleus (MN) formation was highly significant in the NiO-NPs treated group versus the controls. Besides, NiO-NPs treatment resulted in a significant increase in the tail length of comets. Further, electron microscopy revealed a progressive increase in chromatin condensation of the ovarian nurse and follicular cells, in addition to the accumulation of lysosomes and endo-lysosomes in their cytoplasm. In conclusion, NiO-NPs are capable of gaining access to the ovary of B. polycresta and causing DNA damage and a high degree of cellular toxicity in the ovarian cells. The present study highlights, for the first time, the adverse effects of these NPs to female gonads of insects and raised the concern of its genotoxic potential. It would be of interest to investigate NiO-NPs mediated intracellular ROS generation in future studies.


Assuntos
Besouros , Nanopartículas Metálicas , Nanopartículas , Animais , Dano ao DNA , Feminino , Nanopartículas Metálicas/toxicidade , Níquel/toxicidade
3.
Artigo em Inglês | MEDLINE | ID: mdl-33317216

RESUMO

Environmental exposure to low concentrations of heavy metals is common in the general population, but the toxicity, immune response mechanisms, and the effects of single and mixed metal exposures have not been clearly identified. In this study, A549 cells and Raw264.7 cells were exposed to low concentrations of the heavy metals nickel (Ni) and cadmium (Cd) for 24, 48, and 72 h, and then cell viability and cytokine levels were analyzed. We found that exposure to low concentrations of Ni (50 nM) or Cd (10 nM) alone did not affect cell viability. However, mixing them together decreased cell viability. In addition, the levels of IL-10, IL-12, and TNF-α decreased with single (only Cd) and mixed (Ni and Cd) exposures. These results show that exposure to low concentrations of heavy metals could affect the normal immune response, even without obvious clinical manifestations. Therefore, chronic exposure to heavy metals might have adverse effects on overall health.


Assuntos
Cádmio , Sobrevivência Celular , Imunidade , Níquel , Células A549 , Animais , Cádmio/toxicidade , Sobrevivência Celular/efeitos dos fármacos , Exposição Ambiental/efeitos adversos , Humanos , Imunidade/efeitos dos fármacos , Metais Pesados/toxicidade , Camundongos , Níquel/toxicidade , Células RAW 264.7
4.
Ecotoxicol Environ Saf ; 205: 111334, 2020 Dec 01.
Artigo em Inglês | MEDLINE | ID: mdl-32961486

RESUMO

In order to investigate and model toxicity and interactions between metals in mixtures, inhibition of wheat root elongation in response to additions of single-metals of copper (Cu), zinc (Zn), and nickel (Ni) and of binary mixed-metal combinations of Cu-Ni and Zn-Ni was tested, using water culture experiments under different Mg concentrations and pH values. A biotic ligand model (BLM) of single-metal Cu, Zn, and Ni was established. The results showed that the toxicity of Cu, Zn or Ni in isolation decreased with increasing Mg concentration whereas the effects of pH on Cu, Zn, or Ni toxicity were related not only to free Cu2+, Zn2+, and Ni2+ concentrations, but also to inorganic metal complexes. In binary mixtures, the two metals in the Cu-Ni mixture showed a weakly antagonistic effect, whereas the two metals in the Zn-Ni mixture showed greater antagonism. Using data from single-metal Cu, Zn, and Ni BLMs, combined with the toxicity index and the overall amounts of metal ions bound to the biotic ligands, one simple model was developed. This model consisted of the toxic unit (TUM, no competition included) and two extended BLMs, BLM-TUf (f as a function of TU, including competition between Mg2+ and metal ions) and BLM-fmix (including the competition between Mg2+ and metal ions, as well as between free metal ions). They were then used to predict the joint toxicity of Cu-Ni and Zn-Ni binary mixtures to wheat. Both of the extended BLMs could provide more accurate predictions of toxic effects of Cu-Ni and Zn-Ni than TUM. BLM-fmix performed best for the Zn-Ni binary mixture (r2 = 0.93; root-mean-square error, RMSE = 9.87). On the other hand, for the Cu-Ni mixture, the predictive effect based on BLM-TUf (r2 = 0.93; RMSE = 9.60) was similar to that of BLM-fmix (r2 = 0.93; RMSE = 9.56). The results provide a theoretical basis for the evaluation and remediation of soils contaminated with mixtures of heavy metals.


Assuntos
Cobre/toxicidade , Modelos Biológicos , Níquel/toxicidade , Poluentes do Solo/toxicidade , Triticum/efeitos dos fármacos , Zinco/toxicidade , Relação Dose-Resposta a Droga , Antagonismo de Drogas , Ligantes , Raízes de Plantas/efeitos dos fármacos , Raízes de Plantas/crescimento & desenvolvimento , Triticum/crescimento & desenvolvimento
5.
Aquat Toxicol ; 227: 105595, 2020 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-32911330

RESUMO

In order to understand the potential impacts of nickel nanowires (Ni NWs) after reaching the aquatic environment, this research evaluated the toxicity of Ni NWs with different lengths (≤ 1.1, ≤11 and ≤ 80 µm) for several floating, planktonic and nektonic freshwater organisms. In this work, Ni NWs were synthesized by electrodeposition using anodized aluminum oxide (AAO) membranes. The toxicity of the NWs was assessed using a battery of aquatic species representative of key functions at the ecosystem level: the bacterium Aliivibrio fischeri, the algae Raphidocelis subcapitata, the macrophyte Lemna minor, the crustacean Daphnia magna and the zebrafish Danio rerio. Results indicated that for the concentrations tested (up to 2.5 mg L-1) the synthesized Ni NWs showed low toxicity. And although no lethal toxicity was observed for D. magna, at a sublethal level the feeding activity of the freshwater cladoceran was severely affected after exposure to Ni NWs. These findings showed that NWs can be accumulated in the gut of D. magna, even during a short exposure (24 h) directly impairing Daphnia nutrition and eventually populations growth. Consequently, this can also contribute to trophic transfer of NWs along the food chain. According to our results the toxicity of Ni NW may be mainly attributed to physical effects rather than chemical effects of Ni ions, considering that the concentrations of Ni NWs tested in this study were well below the toxicity thresholds reported in the literature for Ni ions and for Ni NMs.


Assuntos
Organismos Aquáticos/efeitos dos fármacos , Nanofios/toxicidade , Níquel/toxicidade , Purificação da Água/métodos , Aliivibrio fischeri , Animais , Clorofíceas , Daphnia/efeitos dos fármacos , Ecossistema , Cadeia Alimentar , Água Doce , Eliminação de Resíduos Líquidos/métodos , Poluentes Químicos da Água/toxicidade , Peixe-Zebra
6.
Nanotoxicology ; 14(8): 1058-1081, 2020 10.
Artigo em Inglês | MEDLINE | ID: mdl-32813574

RESUMO

Nickel nanoparticles (NiNPs) are increasingly used in nanotechnology applications, yet information on sex differences in NiNP-induced lung disease is lacking. The goal of this study was to explore mechanisms of susceptibility between male and female mice after acute or subchronic pulmonary exposure to NiNPs. For acute exposure, male and female mice received a single dose of NiNPs with or without LPS by oropharyngeal aspiration and were necropsied 24 h later. For subchronic exposure, mice received NiNPs with or without LPS six times over 3 weeks prior to necropsy. After acute exposure to NiNPs and LPS, male mice had elevated cytokines (CXCL1 and IL-6) and more neutrophils in bronchoalveolar lavage fluid (BALF), along with greater STAT3 phosphorylation in lung tissue. After subchronic exposure to NiNPs and LPS, male mice exhibited increased monocytes in BALF. Moreover, subchronic exposure of male mice to NiNP only induced higher CXCL1 and CCL2 in BALF along with increased alveolar infiltrates and CCL2 in lung tissue. STAT1 in lung tissue was induced by subchronic exposure to NiNPs in females but not males. Males had a greater induction of IL-6 mRNA in liver after acute exposure to NiNPs and LPS, and greater CCL2 mRNA in liver after subchronic NiNP exposure. These data indicate that susceptibility of males to acute lung inflammation involves enhanced neutrophilia with increased CXCL1 and IL-6/STAT3 signaling, whereas susceptibility to subchronic lung inflammation involves enhanced monocytic infiltration with increased CXCL1 and CCL2. STAT transcription factors appear to play a role in these sex differences. This study demonstrates sex differences in the lung inflammatory response of mice to NiNPs that has implications for human disease.


Assuntos
Pulmão/efeitos dos fármacos , Nanopartículas Metálicas/toxicidade , Níquel/toxicidade , Pneumonia/induzido quimicamente , Caracteres Sexuais , Animais , Líquido da Lavagem Broncoalveolar/citologia , Quimiocina CXCL1/metabolismo , Feminino , Humanos , Exposição por Inalação , Interleucina-6/metabolismo , Pulmão/imunologia , Pulmão/patologia , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Neutrófilos/citologia , Neutrófilos/efeitos dos fármacos , Pneumonia/patologia , Fatores de Transcrição STAT/metabolismo , Transdução de Sinais , Testes de Toxicidade Aguda , Testes de Toxicidade Subcrônica
7.
Aquat Toxicol ; 226: 105556, 2020 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-32652413

RESUMO

Ribosomal (r)DNA is a highly dynamic, conserved, multigene family whose sequence homogeneity is thought to be maintained by intra- and interchromosomal recombination, which are capable of changing rDNA copy number. It is generally not known how environmental stress such as sublethal exposure to environmentally relevant concentrations of metals impacts rDNA copy number. To determine how chronic metal exposure affects rDNA, we measured copy number of the 18S rRNA gene in 355 copper and nickel-exposed samples and 132 metal-free samples derived from 325 mutation accumulation (MA) lines of two genetically distinct Daphnia pulex lineages. The MA lines were sampled at four time points over 100+ generations of clonal propagation. The copy number of rDNA was also measured in 15 individuals sampled from a metal-free non-MA control population established from the same progenitor as one of the MA lineages. We found that mean rDNA copy number fluctuated across lines exposed to metals with a tendency to decrease over time. In contrast, mean rDNA copy number in the metal-free control lines and the non-MA population remained stable over time. It is generally accepted that extreme rDNA loss results in the loss of organism fitness. Thus, fluctuations in rDNA copy number, including losses, could affect the long-term viability of natural populations of Daphnia in metal-contaminated habitats.


Assuntos
Variações do Número de Cópias de DNA/efeitos dos fármacos , DNA Ribossômico/genética , Daphnia/efeitos dos fármacos , Metais Pesados/toxicidade , Acúmulo de Mutações , Poluentes Químicos da Água/toxicidade , Animais , Cobre/toxicidade , Daphnia/genética , Níquel/toxicidade , RNA Ribossômico 18S/genética , Reprodução/efeitos dos fármacos , Reprodução/genética
8.
Chemosphere ; 260: 127627, 2020 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-32673864

RESUMO

Nickel is the most prevailing metal allergen with the highest sensitization rate among the "TOP 25" contact allergens and can affect about 15% of the human population. It is an essential trace metal in plants, animals, and humans. However, the environmental levels of nickel are considerably higher than what is needed for human life. Exposure to high levels of nickel can lead to skin allergies, lung fibrosis, and carcinogenesis. Few existing studies have closely examined the toxicity of nickel, let alone investigated the effective detoxification pathways. Here, we developed a high-throughput screening platform to comprehensively evaluate the nickel toxicity in wild-type C. elegans and explore the underlying detoxification mechanisms in transgenic nematodes. We demonstrated that nickel exerted multiple toxic effects on growth, brood size, feeding, and locomotion in C. elegans. Of which, brood size is the most sensitive endpoint. Nickel was found to first bind to phytochelatin (PC) after entering the worms' body and this PC-Ni complex was further transported by the ABC transporter, CeHMT-1, into the coelomocytes for further detoxification. Our study also demonstrated that the high-throughput screening platform is a promising system for evaluation and investigation of the ecological risks of heavy metals.


Assuntos
Caenorhabditis elegans/fisiologia , Níquel/metabolismo , Transportadores de Cassetes de Ligação de ATP/metabolismo , Animais , Transporte Biológico , Caenorhabditis elegans/metabolismo , Locomoção , Metais Pesados/toxicidade , Nematoides , Níquel/toxicidade , Fitoquelatinas/metabolismo
9.
Ecotoxicol Environ Saf ; 203: 111006, 2020 Oct 15.
Artigo em Inglês | MEDLINE | ID: mdl-32684520

RESUMO

Nickel (Ni) is a widely distributed metal in the environment and an important pollutant because of its many industrial applications. With increasing incidences of Ni contamination, Ni toxicity has become a global public health concern and recent evidence suggests that Ni adversely affects the immune system. Hence, this paper reviews the literature on immune-related effects of Ni exposure, the immunotoxicological effects of Ni, and the underlying mechanism of Ni immunotoxicity. The main focus was on the effect of Ni on the development of organs of immune system, lymphocyte subpopulations, cytokines, immunoglobulins, natural killer (NK) cells, and macrophages. Moreover, Ni toxicity also induces inflammation and several studies demonstrated that Ni could induce immunotoxicity. Excessive Ni exposure can inhibit the development of immune organs by excessively inducing apoptosis and inhibiting proliferation. Furthermore, Ni can decrease T and B lymphocytes, the specific mechanism of which requires further research. The effects of Ni on immunoglobulin A (IgA), IgG, and IgM remain unknown and while Ni inhibited IgA, IgG, and IgM levels in an animal experiment, the opposite result was found in research on humans. Ni inhibits the production of cytokines in non-inflammatory responses. Cytokine levels increased in Ni-induced inflammation responses, and Ni activates inflammation through toll like (TL)4-mediated nuclear factor-κB (NF-κB) and signal transduction cascades mitogen-activated protein kinase (MAPK) pathways. Ni has been indicated to inactivate NK cells and macrophages both in vitro and in vivo. Identifying the mechanisms underlying the Ni-induced immunotoxicity may help to explain the growing risk of infections and cancers in human populations that have been exposed to Ni for a long time. Such knowledge may also help to prevent and treat Ni-related carcinogenicity and toxicology.


Assuntos
Poluentes Ambientais/toxicidade , Sistema Imunitário/efeitos dos fármacos , Níquel/toxicidade , Animais , Apoptose/efeitos dos fármacos , Apoptose/imunologia , Citocinas/metabolismo , Humanos , Sistema Imunitário/crescimento & desenvolvimento , Sistema Imunitário/patologia , Inflamação/induzido quimicamente , Inflamação/metabolismo , Células Matadoras Naturais/efeitos dos fármacos , Células Matadoras Naturais/imunologia , Macrófagos/efeitos dos fármacos , Macrófagos/imunologia , Transdução de Sinais/efeitos dos fármacos , Transdução de Sinais/imunologia
10.
Environ Toxicol ; 35(12): 1308-1317, 2020 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-32681694

RESUMO

Our previous study demonstrated that nano nickel oxide (NiO) induce pulmonary fibrosis in rats and collagen excessive formation in A549 cells, which mechanism was related with the increasing transforming growth factor ß1 (TGF-ß1) secretion. However, it remains unclear understanding the role of TGF-ß1 in collagen excessive formation. Here, we found nano NiO could directly promote epithelial-mesenchymal transition (EMT) via the TGF-ß1/Smads pathway in A549 cells. First, cytotoxicity induced by nano NiO has a dose- and time-dependent manner according to methylthiaozol tetrazolium assay. Second, nano NiO led to the increased contents of type I collagen (Col-I), TGF-ß1, p-Smad2, p-Smad3, alpha-smooth muscle actin (α-SMA), vimentin, and fibronectin, indicating Smads pathway activation and EMT occurence. Third, to verify whether TGF-ß1 activated Smads signaling pathway and EMT occurence, A549 cells were exposed to nano NiO and TGF-ß1 inhibitors (10 µM SB431542). The results showed that TGF-ß1 inhibitors alleviated the nano NiO-induced cytotoxicity and Col-I excessive formation. Meanwhile, TGF-ß1 inhibitors reversed the proteins expression trends of Col-I, p-Smad2, p-Smad3, α-SMA, vimentin, fibronectin, and E-cadherin. These observations suggested that EMT occurrence via TGF-ß1/Smads pathway might play an important role in the collagen excessive formation induced by nano NiO in A549 cells.


Assuntos
Transição Epitelial-Mesenquimal/efeitos dos fármacos , Nanopartículas/toxicidade , Níquel/toxicidade , Proteína Smad2/metabolismo , Proteína Smad3/metabolismo , Fator de Crescimento Transformador beta1/metabolismo , Células A549 , Técnicas de Cultura de Células , Sobrevivência Celular/efeitos dos fármacos , Relação Dose-Resposta a Droga , Humanos , Transdução de Sinais
11.
J Occup Health ; 62(1): e12117, 2020 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-32515878

RESUMO

OBJECTIVE: In this study, in order to investigate the usefulness of intratracheal instillation in assessing the pulmonary toxicity of nanomaterials, intratracheal instillation of nickel oxide-nanoparticles (NiO-NP) was performed. METHODS: In this study, rats were administered test materials by intratracheal instillation at five different research institutions in order to assess the validity of using intratracheal instillation for hazard identification of nanomaterials. Eight-week-old male SD rats were administered NiO-NP dispersed in deionized water by a single intratracheal instillation at doses of 0 (vehicle control), 0.2, 0.67, and 2 mg/kg BW. Three days after instillation, histopathological examination of the lungs was performed. RESULTS: NiO-NP was distributed in the vicinity of hilus of the lung and in the alveoli around the bronchioles. Histopathological changes such as degeneration/necrosis of macrophages, inflammation, and proliferation of type II pneumocyte in the lung were observed, and their severity corresponded with increasing dose. The histopathological observations of pulmonary toxicity were almost similar at each institution. CONCLUSION: The similarity of the histopathological changes observed by five independent groups indicates that intratracheal instillation can be a useful screening method to detect the pulmonary toxicity of nanomaterials.


Assuntos
Exposição por Inalação/efeitos adversos , Pneumopatias/induzido quimicamente , Nanopartículas Metálicas/toxicidade , Níquel/toxicidade , Animais , Masculino , Ratos , Ratos Sprague-Dawley
12.
Ecotoxicol Environ Saf ; 199: 110664, 2020 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-32413645

RESUMO

Crude oil contamination in soils may result in destructive effects on soil microorganisms and plants and act as a source of groundwater contamination. The objective of this study was to evaluate the biological activities for a better understanding of ecological risks. A couple of biological assays, including soil microbial biomass of carbon (SMBC) and urease activity (UA), were used to evaluate the microbial activities in soils. The chemical analysis demonstrated different values of total petroleum hydrocarbons (TPHs) concentrations (from 0.12 to 2.99 mg/kg of dry soil) and relatively high quantities of Nickel (from 32 to 136.8 mg/kg of dry soil) and cadmium (from 0 to 4 mg/kg of dry soil) in samples. UA and SMBC values were comparatively lower in close distances to oil wells, pipelines, and especially drilling sediments pool. The spatial variability maps using the interpolation module by GIS specified the line from northwest to the southeast of the area as a more affected area by TPHs and Ni + Cd.


Assuntos
Carbono/análise , Hidrocarbonetos/toxicidade , Campos de Petróleo e Gás , Petróleo/toxicidade , Microbiologia do Solo , Poluentes do Solo/toxicidade , Urease/metabolismo , Biodegradação Ambiental , Biomassa , Cádmio/análise , Cádmio/toxicidade , Hidrocarbonetos/análise , Irã (Geográfico) , Níquel/análise , Níquel/toxicidade , Petróleo/análise , Solo/química , Poluentes do Solo/análise
13.
Chemosphere ; 255: 126913, 2020 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-32402875

RESUMO

Nickel nanoparticles (Ni NPs) have a wide range of application prospects, but there is still a lack of their safety evaluation for the reproductive system. Nowadays, male reproductive health has been widely concerned because of the increasing incidence of male infertility. Studies have shown that Ni NPs can cause male reproductive toxicity. The purpose of this study was to investigate the toxicity of Ni NPs on GC-1 cells, a mouse spermatogonia cell line, and to explore the possible mechanism underlying the induction of apoptosis via PI3K/AKT/mTOR signaling pathway. The cell ultrastructure was firstly observed under a transmission electron microscope. Then, cell proliferation, cycle and apoptosis were detected by CCK-8 and flow cytometry, respectively. Furthermore, the expression levels of related proteins and genes were determined by Western blot and Reverse transcription-polymerase chain reaction, respectively. The results showed that Ni NPs could not only cause changes in cell ultrastructure, decreased survival rate and arrested G1 phase cell cycle, but also activated apoptosis pathway by inhibiting the PI3K/AKT/mTOR signaling pathway. The results of this study provide novel insights to explore the mechanisms of reproductive toxicity of Ni NPs and are of great significance to develop safety evaluation criteria for Ni NPs.


Assuntos
Nanopartículas Metálicas/toxicidade , Níquel/toxicidade , Acetatos , Animais , Apoptose/efeitos dos fármacos , Linhagem Celular , Proliferação de Células/efeitos dos fármacos , Humanos , Masculino , Camundongos , Fenóis , Fosfatidilinositol 3-Quinases/metabolismo , Proteínas Proto-Oncogênicas c-akt/metabolismo , Transdução de Sinais/efeitos dos fármacos , Serina-Treonina Quinases TOR/metabolismo
14.
Ecotoxicol Environ Saf ; 197: 110593, 2020 Jul 01.
Artigo em Inglês | MEDLINE | ID: mdl-32294596

RESUMO

Arable land contamination with nickel (Ni) has become a major threat to worldwide crop production. Recently, melatonin has appeared as a promising stress-relief substance that can alleviate heavy metal-induced phytotoxicity in plants. However, the plausible underlying mechanism of melatonin function under Ni stress has not been fully substantiated in plants. Herein, we conducted an experiment that unveiled critical mechanisms in favor of melatonin-mediated Ni-stress tolerance in tomato. Ni stress markedly inhibited growth and biomass by impairing the photosynthesis, photosystem function, mineral homeostasis, root activity, and osmotic balance. In contrast, melatonin application notably reinforced the plant growth traits, increased photosynthesis efficiency in terms of chlorophyll content, upregulation of chlorophyll synthesis genes, i.e. POR, CAO, CHL G, gas exchange parameters, and PSII maximum efficiency (Fv/Fm), decreased Ni accumulation and increased mineral nutrient homeostasis. Moreover, melatonin efficiently restricted the hydrogen peroxide (H2O2) and superoxide radical production and increased RBOH expression and restored cellular integrity (less malondialdehyde and electrolyte leakage) through triggering the antioxidant enzyme activities and modulating AsA-GSH pools. Notably, oxidative stress was effectively mitigated by upregulation of several defense genes (SOD, CAT, APX, GR, GST, MDHAR, DHAR) and melatonin biosynthesis-related genes (TDC, T5S, SNAT, ASMT). Besides, melatonin treatment enhanced secondary metabolites (phenols, flavonoids, and anthocyanin) contents along with their encoding genes (PAL, CHS) expression, and these metabolites potentially restricted excess H2O2 accumulation. In conclusion, our findings deciphered the potential functions of melatonin in alleviating Ni-induced phytotoxicity in tomato through boosting the biomass production, photosynthesis, nutrient uptake, redox balance, and secondary metabolism.


Assuntos
Antioxidantes/farmacologia , Lycopersicon esculentum/efeitos dos fármacos , Melatonina/farmacologia , Níquel/toxicidade , Poluentes do Solo/toxicidade , Antioxidantes/metabolismo , Lycopersicon esculentum/crescimento & desenvolvimento , Lycopersicon esculentum/metabolismo , Melatonina/metabolismo , Níquel/metabolismo , Oxirredução/efeitos dos fármacos , Estresse Oxidativo/efeitos dos fármacos , Estresse Oxidativo/genética , Fotossíntese/efeitos dos fármacos , Metabolismo Secundário/efeitos dos fármacos , Metabolismo Secundário/genética , Plântula/efeitos dos fármacos , Plântula/crescimento & desenvolvimento , Plântula/metabolismo , Poluentes do Solo/metabolismo
15.
Biochem Biophys Res Commun ; 526(4): 920-926, 2020 06 11.
Artigo em Inglês | MEDLINE | ID: mdl-32279993

RESUMO

Ovarian cancer G protein-coupled receptor 1 (OGR1), also known as GPR68, is a proton-sensing G protein-coupled receptor (GPCR) coupling to Gq/11/phospholipase C/Ca2+ signaling pathways. The specific histidine residues at the extracellular surface of OGR1 are suggested to be involved in the proton sensing. Later, some metal ions, including nickel ion (Ni2+), are also indicated to be OGR1 ligands. OGR1 polymorphic variants have recently been found in three families with amelogenesis imperfecta, which suggested that OGR1 is required for the process of dental enamel formation. One of these families possesses a missense mutation from leucine to proline at 74 (L74P) of OGR1. In the present study, we characterized HEK293 cells with L74P OGR1 (L74P-OGR1) and hemagglutinin (HA)-tag, as compared with cells with wild-type OGR1 (WT-OGR1) and HA-tag. We found that either acidic pH or NiCl2 induced intracellular Ca2+ mobilization and morphological change in WT-OGR1-transfected cells; however, the extracellular stimulus-induced actions were severely damaged in L74P-OGR1-transfected cells. We further confirmed that either WT-OGR1 or L74P-OGR1 is localized mainly in the surface of the cells, but only WT-OGR1 is internalized in response to acidification or NiCl2. Thus, the L74P-OGR1 protein may be distributed in the plasma membranes but severely damaged in the receptor functions. We speculate that L74P in the second transmembrane domain in OGR1 may result in conformational changes in the receptor, thereby disturbing the sensing extracellular signals, i.e., protons or metal ions, and/or transducing them to the intracellular signaling machinery through G proteins.


Assuntos
Amelogênese Imperfeita/genética , Amelogênese Imperfeita/metabolismo , Mutação de Sentido Incorreto/genética , Receptores Acoplados a Proteínas-G/genética , Sinalização do Cálcio , Forma Celular/efeitos dos fármacos , Endocitose/efeitos dos fármacos , Células HEK293 , Humanos , Concentração de Íons de Hidrogênio , Lisofosfolipídeos/farmacologia , Níquel/toxicidade , Estrutura Secundária de Proteína , RNA Mensageiro/genética , RNA Mensageiro/metabolismo , Receptores Acoplados a Proteínas-G/química , Receptores Acoplados a Proteínas-G/metabolismo
16.
BMC Genomics ; 21(1): 214, 2020 Mar 06.
Artigo em Inglês | MEDLINE | ID: mdl-32143559

RESUMO

BACKGROUND: Cupriavidus strain STM 6070 was isolated from nickel-rich soil collected near Koniambo massif, New Caledonia, using the invasive legume trap host Mimosa pudica. STM 6070 is a heavy metal-tolerant strain that is highly effective at fixing nitrogen with M. pudica. Here we have provided an updated taxonomy for STM 6070 and described salient features of the annotated genome, focusing on heavy metal resistance (HMR) loci and heavy metal efflux (HME) systems. RESULTS: The 6,771,773 bp high-quality-draft genome consists of 107 scaffolds containing 6118 protein-coding genes. ANI values show that STM 6070 is a new species of Cupriavidus. The STM 6070 symbiotic region was syntenic with that of the M. pudica-nodulating Cupriavidus taiwanensis LMG 19424T. In contrast to the nickel and zinc sensitivity of C. taiwanensis strains, STM 6070 grew at high Ni2+ and Zn2+ concentrations. The STM 6070 genome contains 55 genes, located in 12 clusters, that encode HMR structural proteins belonging to the RND, MFS, CHR, ARC3, CDF and P-ATPase protein superfamilies. These HMR molecular determinants are putatively involved in arsenic (ars), chromium (chr), cobalt-zinc-cadmium (czc), copper (cop, cup), nickel (nie and nre), and silver and/or copper (sil) resistance. Seven of these HMR clusters were common to symbiotic and non-symbiotic Cupriavidus species, while four clusters were specific to STM 6070, with three of these being associated with insertion sequences. Within the specific STM 6070 HMR clusters, three novel HME-RND systems (nieIC cep nieBA, czcC2B2A2, and hmxB zneAC zneR hmxS) were identified, which constitute new candidate genes for nickel and zinc resistance. CONCLUSIONS: STM 6070 belongs to a new Cupriavidus species, for which we have proposed the name Cupriavidus neocaledonicus sp. nov.. STM6070 harbours a pSym with a high degree of gene conservation to the pSyms of M. pudica-nodulating C. taiwanensis strains, probably as a result of recent horizontal transfer. The presence of specific HMR clusters, associated with transposase genes, suggests that the selection pressure of the New Caledonian ultramafic soils has driven the specific adaptation of STM 6070 to heavy-metal-rich soils via horizontal gene transfer.


Assuntos
Cupriavidus/efeitos dos fármacos , Cupriavidus/genética , Metais Pesados/toxicidade , Mimosa/microbiologia , Cádmio/metabolismo , Família Multigênica , Níquel/toxicidade , Filogenia , RNA Ribossômico 16S/genética , Rhizobium/efeitos dos fármacos , Rhizobium/genética , Solo , Microbiologia do Solo , Simbiose , Sintenia/genética , Zinco/toxicidade
17.
Biochem Biophys Res Commun ; 526(1): 117-121, 2020 05 21.
Artigo em Inglês | MEDLINE | ID: mdl-32197839

RESUMO

Tannic acid (TA) is a polyphenol compound present in wines and many beverages. Although previous works have shown that TA could cause vasodilation in an endothelial cell (EC)-dependent manner, there is hitherto no report showing whether TA could raise EC cytosolic Ca2+ concentration. In this work we examined the effects of TA on cytosolic Ca2+ of mouse brain bEND.3 EC. TA (1-30 µM) caused a slow elevation in cytosolic Ca2+ level in a concentration-dependent manner. At 30 µM, TA triggered Ca2+ influx without causing intracellular Ca2+ release. TA-triggered Ca2+ influx was suppressed by Ni2+ (a non-specific Ca2+ channel blocker), ruthenium red and SKF 96365 (non-specific TRP channel blockers), CBA (a selective TRPM4 inhibitor) and M 084 (a selective TRPC4/C5 blocker). However, TA-triggered Ca2+ influx pathway was not permeable to Mn2+. Our results suggest TA activated TRP channels, possibly TRPM4 and TRPC4/C5, to promote influx of Ca2+.


Assuntos
Bebidas/análise , Cálcio/metabolismo , Células Endoteliais/metabolismo , Taninos/análise , Canais de Receptores Transientes de Potencial/metabolismo , Vasodilatadores/análise , Vinho/análise , Animais , Sinalização do Cálcio/efeitos dos fármacos , Células Endoteliais da Veia Umbilical Humana/efeitos dos fármacos , Células Endoteliais da Veia Umbilical Humana/metabolismo , Humanos , Imidazóis/farmacologia , Manganês/metabolismo , Camundongos , Níquel/toxicidade , Rutênio Vermelho/farmacologia , Canais de Receptores Transientes de Potencial/antagonistas & inibidores
18.
Biochim Biophys Acta Biomembr ; 1862(8): 183250, 2020 08 01.
Artigo em Inglês | MEDLINE | ID: mdl-32126229

RESUMO

Anthropogenic activity has increased human exposure to metals and resulted in metal induced toxicity. Essential trace elements like cobalt (Co), nickel (Ni), and manganese (Mn) are best known for their roles as important cofactors in many enzymes involved in signalling, metabolism, and response to oxidative stress. However, deficiencies as well as long-term overexposure to these metals can result in negative health effects. Co has been associated with cardiomyopathy, lung disease, and hearing damage, while Ni is a known carcinogen, as well as a common sensitizing metal. Mn is best classified as a neurotoxicant that causes a disorder alike to idiopathic Parkinson's disease known as Manganism. Although the mechanisms of Co, Ni, and Mn toxicity are complex and have yet to be fully elucidated, research over the years has provided useful insights into understanding metal-induced detrimental effects at the cellular and molecular level. One area of research that has been explored in less detail are metal interactions with lipids and biological membranes, which are a potentially critical target as membranes are the first point of contact for cells. This review covers the current understandings of Co, Ni and Mn toxicity, in terms of human exposure, homeostasis and mechanisms of transport, potential cellular targets, and, of primary focus, metal interactions with lipid and biomembranes. A variety of effects like membrane rigidification, leakage affecting membrane potentials, lipid phase changes, alterations in lipid metabolism and changes of cellular morphology illustrate the vast potential for metal-based membrane effects contributing to their toxicity.


Assuntos
Membrana Celular/efeitos dos fármacos , Lipídeos/química , Metais Pesados/toxicidade , Estresse Oxidativo/efeitos dos fármacos , Membrana Celular/química , Cobalto/toxicidade , Homeostase/efeitos dos fármacos , Humanos , Manganês/toxicidade , Níquel/toxicidade
19.
Chemosphere ; 248: 125926, 2020 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-32006827

RESUMO

We examined effects of the three metals cadmium (Cd), copper (Cu), and nickel (Ni) on two subpopulations of the cyclopoid copepod Paracyclopina nana. We sought to investigate the effects of metal exposure on population growth and structure of P. nana and to understand the parameters affecting the metal bioaccumulation in copepods. A first experiment tested the hypothesis of competition between these metals in a mixture using a P. nana mass culture in 10 L beakers with the sublethal concentrations (1/3 of LC50) as determined for E. affinis. A second experiment pursued the same with a P. nana population which was adapted to a higher Cu concentration for several generations (226.9 ± 15.9 µg g-1 dw Cu in copepods) and using the proper sublethal concentrations for P. nana. After 96 h of exposure, results from the first experiment showed a decreasing population growth and instead of an increasing metal accumulation in copepods. Cd also appeared to be more accumulated when it was alone, confirming the hypothesis of metal competition in mixture. Results from the second experiment revealed less marked effects. When metal concentrations increased in the treatment it decreased in copepods, indicating depuration activity in the population already adapted to metal exposure. This paper is the first one investigating the parameters affecting the bioaccumulation capacity of P. nana in response to metals. It offers a better understanding of copepod responses to metal contamination in a complex aquatic environment.


Assuntos
Copépodes/fisiologia , Metais/toxicidade , Poluentes Químicos da Água/toxicidade , Animais , Bioacumulação , Cádmio/toxicidade , Copépodes/efeitos dos fármacos , Copépodes/crescimento & desenvolvimento , Cobre/toxicidade , Níquel/toxicidade , Crescimento Demográfico
20.
Chemosphere ; 249: 126121, 2020 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-32065994

RESUMO

Metal accumulation in soil could lead to severe damage to plants, animals, and humans. The present work aims to evaluate the effects of nickel (Ni) exposure on Medicago sativa at physiological, biochemical, and transcriptomic levels. Plants were exposed to five increasing concentrations of Ni (0, 50, 150, 250, and 500 mg/kg) for 60 days. Agronomic parameters (fresh and dry matter) and chlorophyll content (Chl) were determined in an alfalfa plant. Chemical analyses were conducted, involving the determination of Ni loads in plants (roots and shoots). Moreover, malondialdehyde accumulation (MDA), glutathione-S-transferase (GST), and peroxidase activities, termed as oxidative stress biomarkers, were measured. The gene expression levels of Prx1C, GST, and phytochelatins (PCs) were determined at different nickel concentrations. Our results showed that Ni concentration in plants increased significantly along with Ni concentration in the soil. Regarding oxidative stress biomarkers, Ni contamination caused an increase in peroxidase and GST activities, with a remarkable accumulation of MDA, especially for the highest Ni concentration (500 mg/kg of Ni). Our data showed also a significant upregulation of Prx1C and GST genes in shoots and roots. The PCs' gene expression was significantly enhanced in response to the different nickel concentrations, suggesting their important role in Ni detoxification in alfalfa plants. Our data provided evidence about the clear toxicity of Ni, an often-underestimated trace element.


Assuntos
Medicago sativa/fisiologia , Níquel/toxicidade , Poluentes do Solo/toxicidade , Animais , Clorofila/metabolismo , Malondialdeído/metabolismo , Medicago sativa/efeitos dos fármacos , Oxirredução , Estresse Oxidativo/efeitos dos fármacos , Peroxidase/metabolismo , Peroxidases/metabolismo , Fitoquelatinas/metabolismo , Raízes de Plantas/metabolismo , Solo/química , Poluentes do Solo/metabolismo , Transcriptoma/efeitos dos fármacos
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