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1.
Ecotoxicol Environ Saf ; 181: 572-578, 2019 Oct 15.
Artigo em Inglês | MEDLINE | ID: mdl-31252212

RESUMO

Arsenic (As) and sulfur dioxide (SO2) are two environmental pollutants that have been shown to promote the development of human cancer. In recent years, due to increased pollution, humans are often exposed to SO2, in addition to As. Despite the development and implementation of standards for environment and air quality, cases of disease caused by As or SO2 continue to rise alarmingly. It is currently unknown whether simultaneous exposure to As and SO2 results in increased cancer promoting activity. In this study, concentrations of As and SO2 below the limits established by the world health organization (WHO) in force environmental standards (concentrations of As should be lower than 1×10-2 mg/L and SO2 should be lower than 50 µg/m3), were employed to investigate possible, long-term, synergistic effects of As and SO2, by using cell-based assays. We found that co-exposure to these pollutants significantly promotes HepG2 cancer cell migration, while As or SO2 alone have no remarkable effects. Integrins αvß3 play a key role in this process, as cilengitide, an integrin αvß3 inhibitor, substantially prevented As and SO2-induced cell migration. MMPs, IL-8, and TGF-ß were also involved in the induced cell migration. In summary, combined exposure to As and SO2 promotes integrin-dependent cell migration and may be of relevance for the activation of mechanisms underlying liver cancer progression.

2.
Ecotoxicol Environ Saf ; 178: 9-16, 2019 Aug 30.
Artigo em Inglês | MEDLINE | ID: mdl-30980964

RESUMO

Recently, sulfur dioxide (SO2) has been considered to be a beneficial bio-regulator in animals. However, the positive roles of SO2 in plant adaptation to drought stress are still unclear. In this study, we investigated the physiological and molecular changes that are induced by SO2 fumigation to improve the drought tolerance of foxtail millet seedlings. The relative water content in the leaves of drought-stressed seedlings was significantly improved by pre-exposure to 30 mg/m3 SO2. These responses might be related to decreased stomatal apertures and a reduced leaf transpiration rate, which were induced by SO2 under drought conditions. In addition, the SO2 pretreatment markedly enhanced proline accumulation in the leaves of drought-stressed seedlings, which was supported by increased Δ1-pyrroline-5-carboxylate synthetase (P5CS) activity, decreased proline dehydrogenase (ProDH) activity, and the corresponding transcripts. Moreover, the SO2 application upregulated the enzyme activity of catalase (CAT) and peroxidase (POD) in the leaves of drought-stressed plants, as well as their transcripts, which contributed to the scavenging of hydrogen peroxide (H2O2) and alleviated drought-induced oxidative damage, as indicated by the decreased malondialdehyde (MDA) level in SO2-pretreated plants. Together, these results indicate that the application of SO2 might enhance drought tolerance by reducing stomatal apertures, increasing proline accumulation, and promoting antioxidant defence in foxtail millet seedlings. This study presents new insight into the beneficial roles of SO2 in plant responses to drought stress.


Assuntos
Adaptação Fisiológica/efeitos dos fármacos , Secas , Fumigação , Setaria (Planta)/efeitos dos fármacos , Dióxido de Enxofre/farmacologia , Antioxidantes/metabolismo , Prolina/metabolismo , Plântula/efeitos dos fármacos , Plântula/crescimento & desenvolvimento , Plântula/metabolismo , Setaria (Planta)/crescimento & desenvolvimento , Setaria (Planta)/metabolismo , Estresse Fisiológico/efeitos dos fármacos
3.
Chemosphere ; 224: 280-288, 2019 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-30825854

RESUMO

Although emerging evidence suggests positive association of arsenic (As) or sulfur dioxide (SO2) exposure with human diseases, reports concerning the effects of co-exposure of As and SO2 are lacking. Moreover, there is insufficient information in the literature about As and SO2 co-exposure to renal injury. In this study, we focus on the environmental problems of excessive As and SO2 that co-exist in many coal consumption areas. We used both C57BL/6 mice and 293T cells to detect toxicities of As and SO2 exposure alone or in combination. Our results showed that co-exposure significantly increased the hazard compared with exposure to As or SO2 alone. Mouse kidney tissue slices showed that co-exposure caused more severe diffuse sclerosing glomerulonephritis than As and SO2 exposure alone. Meanwhile experiments showed that apoptosis was aggravated by co-exposure of As and SO2 in 293T cells. Because As and SO2 cause cell toxicity through increasing oxidative stress, next we detected ROS and other oxidative stress parameters, and the results showed oxidative stress was increased by co-exposure compared with the other three groups. The expression levels of downstream genes in the NF-κB and caspase pathways were higher in the co-exposure group than in the groups of As or SO2 exposure alone in mice and 293T cells. Based on the above results, co-exposure could induce higher toxicity in vitro and in vivo compared with single exposure to As or SO2, indicating that people living in places that contaminated by As and SO2 may have higher chance to get renal injury.


Assuntos
Arsenitos/toxicidade , Poluentes Ambientais/toxicidade , Nefropatias/induzido quimicamente , Rim/efeitos dos fármacos , NF-kappa B/metabolismo , Compostos de Sódio/toxicidade , Dióxido de Enxofre/toxicidade , Animais , Apoptose/efeitos dos fármacos , Sobrevivência Celular/efeitos dos fármacos , Sinergismo Farmacológico , Células HEK293 , Humanos , Rim/metabolismo , Rim/patologia , Nefropatias/metabolismo , Nefropatias/patologia , Masculino , Camundongos Endogâmicos C57BL , Estresse Oxidativo/efeitos dos fármacos , Transdução de Sinais
4.
Toxicology ; 2018 Sep 29.
Artigo em Inglês | MEDLINE | ID: mdl-30278210

RESUMO

Inorganic arsenic (iAs), a ubiquitous element and a natural drinking water contaminant, has been found to impair male reproductive function. However, the effect of long-term exposure to arsenic on testis damage and its underlying mechanisms still require further evaluation. In the study, male C57BL/6 mice (4 weeks) were treated with sodium arsenite at the doses of 5 or 50 ppm arsenic via drinking water for 180 days. Sperm count, histology in testes, oxidative stress biomarkers, cell cycle progress and apoptosis were assessed. Our results showed that arsenite seriously destroyed the structure of the testes and reduced the sperm count. Arsenite significantly decreased the activity of total superoxide dismutase (T-SOD) and glutathione (GSH) content but increased the levels of reactive oxygen species (ROS) and malondialdehyde (MDA) in testes. Furthermore, arsenite could induce G2/M phase arrest in testes, concurrent with a significant decrease in mRNA and protein levels of cdc2 and cyclin B1, the upregulation of p-cdc2, and an increase in mRNA levels of p53 and p21. Arsenite induced testicular apoptosis with a significant increase in Bax mRNA and protein levels, especially the caspase-3 activation. Testicular toxicity of the high dose group was stronger than that of the low dose group. In conclusion, testicular toxicity due to long-term exposure to arsenite may relate to oxidative damage, G2/M arrest and promoted apoptosis in the testes of mice, which contributed to the increased risk of spermatogenesis disorders and male infertility.

5.
Environ Toxicol Pharmacol ; 63: 84-91, 2018 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-30189373

RESUMO

Arsenic (As) has been recognized as a cause of male reproductive toxicity. However, effects of long-term arsenic exposure (puberty-adult) on spermatogenesis, testosterone synthesis, and the expression of androgen binding protein (ABP) and Ddx3y remain unclear. The objective of this investigation was to explore these effects and the underlying mechanisms. Male mice were treated with 5 and 50 ppm arsenic for 6 months via drinking water. The results showed that arsenic reduced sperm count and sperm motility and enhanced the abnormal sperm percentage. The decrease in the number of spermatogenic cells and sperm in seminiferous tubules and the decline in the Johnsen score were observed in both arsenic-treated groups, suggesting spermatogenesis disorders. Moreover, arsenic diminished serum testosterone, along with the reduced expression of luteinizing hormone receptor (LHR), steroidogenic acute regulatory protein (StAR) and 17-ß-hydroxysteroid dehydrogenase (17ß-HSD) genes. Arsenic also down-regulated mRNA levels of ABP and Ddx3y in a dose-dependent manner. Meanwhile, the protein levels of StAR, 17ß-HSD and Ddx3y were significantly reduced in arsenic-treated groups. Taken together, these results suggest that the reduced testosterone through inhibition of the expression of multiple genes responsible for the biosynthesis, the damaged androgen homeostasis partially via lessening the expression levels of the ABP gene and the down-regulated expression of Ddx3y, may contribute to spermatogenesis disorders in mice exposed to arsenic.

6.
Ecotoxicol Environ Saf ; 165: 164-173, 2018 Dec 15.
Artigo em Inglês | MEDLINE | ID: mdl-30195209

RESUMO

As two potential environmental hazards, sulphur dioxide (SO2) and arsenic have adverse effects on male reproduction, but the mechanism of which and their combined toxicity are not clear. In this study, we investigate male reproductive toxicity with a focus on spermatogenesis by treating mice with 5 mg/m3 SO2 and/or 5 mg/L arsenic. Our results showed that arsenic exposure caused significant decreases in water and food consumption and body weight in mice, whereas these changes were not observed in the SO2-only group. Both SO2 and arsenic reduced sperm counts, increased the percentage of sperm malformation, and induced abnormal testicular pathological changes. Elevated H2O2 and MDA contents, declined T-SOD activity, decreased spermatogenic cell counts, enhanced caspase-3 activity, and increased TUNEL-positive cells were also observed in mice exposed to SO2 and/or arsenic. Moreover, SO2 and arsenic co-exposure changed the mRNA levels of Bax and Bcl-2, decreased serum testosterone levels, and downregulated the expression of steroidogenic-related genes (LHR, StAR, and ABP) in mice. These findings provide a new theoretical basis for understanding how SO2 and arsenic interfere with spermatogenesis leading to infertility. These results also suggest that SO2 and arsenic co-exposure likely result in an additive effect on male reproductive toxicity in mice.

7.
Brain Behav Immun ; 71: 23-27, 2018 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-29678794

RESUMO

Inflammatory bowel disease (IBD) is a debilitating immune-related condition that affects over 1.4 million Americans. Recent studies indicate that taste receptor signaling is involved in much more than sensing food flavor, and taste receptors have been localized in a variety of extra-oral tissues. One of the newly revealed functions of taste receptors and downstream signaling proteins is modulation of immune responses to microbes and parasites. We previously found that components of the taste receptor signaling pathway are expressed in subsets of the intestinal epithelial cells. α-Gustducin, a key G-protein α subunit involved in sweet, umami, and bitter taste receptor signaling, is expressed in the intestinal mucosa. In this study, we investigated the role of α-gustducin in regulation of gut mucosal immunity and inflammation using α-gustducin knockout mice in the dextran sulfate sodium (DSS)-induced IBD model. DSS is a chemical colitogen that can cause intestinal epithelial damage and inflammation. We analyzed DSS-induced colitis in α-gustducin knockout versus wild-type control mice after administration of DSS in drinking water. Our results show that the knockout mice had aggravated weight loss, diarrhea, intestinal bleeding, and inflammation over the experimental period compared to wild-type mice, concurrent with augmented immune cell infiltration and increased expression of TNF and IFN-γ but decreased expression of IL-13 and IL-5 in the colon. These results suggest that the taste receptor signaling pathway may play critical roles in regulating gut immune balance and inflammation.

8.
Ecotoxicol Environ Saf ; 157: 207-215, 2018 Aug 15.
Artigo em Inglês | MEDLINE | ID: mdl-29625394

RESUMO

Sulfur dioxide (SO2) was recently proposed as a novel bio-regulator in mammals. However, the possible advantageous effects of SO2 in plant adaptation to heavy metal-contaminated environments are largely unknown. In the present study, using Na2SO3/NaHSO3 derivatives as SO2 donors, we investigated the possible roles and regulation mechanisms of SO2 in alleviating Cd2+ toxicity in foxtail millet seedlings. Exogenous SO2 derivatives (0.5 mM) application significantly reduced the seedling growth inhibition caused by Cd2+ stress. Cd2+-induced oxidative damage was also alleviated by SO2 derivatives, which was supported by the decreased malondialdehyde (MDA) level in the leaves of seedlings pretreated with SO2 derivatives. These responses were related to the enhanced activities of representative antioxidant enzymes, including catalase and superoxide dismutase, as well as the up-regulation of ascorbate-glutathione cycle, which contributed to the scavenging of Cd2+-elicited O2•- and H2O2 within the leaves of foxtail millet seedlings. Also, SO2 derivative application promoted sulfur assimilation and increased the content of glutathione and phytochelatins, which may help to enhance Cd2+ detoxification capacity in foxtail millet seedlings. Moreover, application of SO2 derivatives caused down-regulation of the transcript expression levels of several genes involved in Cd2+ uptake and translocation, such as NRAMP1, NRAMP6, IRT1, IRT2, HMA2, and HMA4, thus resulting in reduced Cd2+ accumulation in the shoots and roots of Cd2+-stressed seedlings. Collectively, these results suggest that exogenous SO2 derivative application can alleviate oxidative damage and restrict Cd2+ buildup, thereby reducing Cd2+-induced growth inhibition in foxtail millet seedlings upon Cd2+ exposure. This novel finding indicates that the usage of SO2 derivatives may be an effective approach for enhancing Cd2+ tolerance in foxtail millet and other crops.


Assuntos
Cádmio/toxicidade , Poluentes Ambientais/toxicidade , Estresse Oxidativo/efeitos dos fármacos , Setaria (Planta)/efeitos dos fármacos , Sulfitos/farmacologia , Antioxidantes/metabolismo , Cádmio/metabolismo , Catalase/metabolismo , Regulação da Expressão Gênica de Plantas/efeitos dos fármacos , Glutationa/metabolismo , Malondialdeído/metabolismo , Fitoquelatinas/metabolismo , Plântula/efeitos dos fármacos , Plântula/crescimento & desenvolvimento , Plântula/metabolismo , Setaria (Planta)/crescimento & desenvolvimento , Setaria (Planta)/metabolismo , Superóxido Dismutase/metabolismo
9.
Ecotoxicol Environ Saf ; 147: 523-529, 2018 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-28917191

RESUMO

Sulfur dioxide (SO2) is a common air pollutant that has complex impacts on plants. The effect of prior exposure to 30mgm-3 SO2 on defence against Botrytis cinerea (B. cinerea) in Arabidopsis thaliana and the possible mechanisms of action were investigated. The results indicated that pre-exposure to 30mgm-3 SO2 resulted in significantly enhanced resistance to B. cinerea infection. SO2 pre-treatment significantly enhanced the activities of defence-related enzymes including phenylalanine ammonia-lyase (PAL), polyphenol oxidase (PPO), ß-1,3-glucanase (BGL) and chitinase (CHI). Transcripts of the defence-related genes PAL, PPO, PR2, and PR3, encoding PAL, PPO, BGL and CHI, respectively, were markedly elevated in Arabidopsis plants pre-exposed to SO2 and subsequently inoculated with B. cinerea (SO2+ treatment group) compared with those that were only treated with SO2 (SO2) or inoculated with B. cinerea (CK+). Moreover, SO2 pre-exposure also led to significant increases in the expression levels of MIR393, MIR160 and MIR167 in Arabidopsis. Meanwhile, the expression of known targets involved in the auxin signalling pathway, was negatively correlated with their corresponding miRNAs. Additionally, the transcript levels of the primary auxin-response genes GH3-like, BDL/IAA12, and AXR3/IAA17 were markedly repressed. Our findings indicate that 30mgm-3 SO2 pre-exposure enhances disease resistance against B. cinerea in Arabidopsis by priming defence responses through enhancement of defence-related gene expression and enzyme activity, and miRNA-mediated suppression of the auxin signalling pathway.


Assuntos
Arabidopsis/microbiologia , Botrytis/crescimento & desenvolvimento , Resistência à Doença/efeitos dos fármacos , Doenças das Plantas/prevenção & controle , Dióxido de Enxofre/farmacologia , Arabidopsis/genética , Arabidopsis/metabolismo , Resistência à Doença/genética , Regulação da Expressão Gênica de Plantas/efeitos dos fármacos , Genes de Plantas , MicroRNAs/genética , Doenças das Plantas/genética , Doenças das Plantas/microbiologia
10.
Toxicol Lett ; 285: 43-50, 2018 Mar 15.
Artigo em Inglês | MEDLINE | ID: mdl-29288730

RESUMO

Sulfur dioxide (SO2) is one of potential risk factors for induction and/or exacerbation of asthma, but the underlying mechanisms are not well understood. In this study, we investigate the role of SO2 in asthma using a classical asthmatic model with allergic airway inflammation by treating C57BL/6 mice with ovalbumin (OVA) and/or 10 mg/m3 SO2. Our results showed that SO2 exposure alone induced slight pathological changes but did not significantly increase inflammatory cell counts, pro-inflammatory cytokine expression, and mucus production in the airway of mice, whereas SO2 exposure in OVA-induced asthmatic mice caused marked pulmonary pathological changes and significantly increased the counts of eosinophil-rich leukocytes compared with OVA alone asthmatic mice. The expression of MUC5AC, TNF-α, Th2 cytokines (IL-4, IL-5, and IL-13) and STAT6 was further up-regulated in OVA plus SO2 treated mice compared with OVA alone treated mice. In addition, exposure to SO2 alone markedly elevated STAT6 mRNA levels and hydrogen peroxide (H2O2) content in the lung. These findings suggest that SO2 amplifies Th2 inflammatory responses in OVA-induced asthmatic mice by activating STAT6, which can further induce Th2 cytokine expression. Induction of STAT6 expression might be an important mechanism underlying the increased risk for asthma after environmental exposure.


Assuntos
Poluentes Atmosféricos/toxicidade , Asma/imunologia , Fator de Transcrição STAT6/biossíntese , Dióxido de Enxofre/toxicidade , Células Th2/efeitos dos fármacos , Animais , Citocinas/biossíntese , Citocinas/imunologia , Modelos Animais de Doenças , Pulmão/efeitos dos fármacos , Pulmão/imunologia , Masculino , Camundongos Endogâmicos C57BL , Ovalbumina/administração & dosagem , Estresse Oxidativo/efeitos dos fármacos , Estresse Oxidativo/imunologia , RNA Mensageiro/metabolismo , Transdução de Sinais , Células Th2/imunologia
11.
World J Microbiol Biotechnol ; 34(1): 8, 2017 Dec 13.
Artigo em Inglês | MEDLINE | ID: mdl-29236189

RESUMO

Fertilization is a key agricultural practice for increasing millet yields and influencing soil properties, enzyme activities and rhizosphere bacterial communities. High throughput Illumina sequencing of the 16S rDNA was applied to compare the bacterial community structures and diversities among six different soil samples. The experiments involved the following: no fertilizer (CK), phosphate (P) and potassium (K) plus organic manure (M) (PKM), nitrogen (N) and K plus M (NKM), NPM, NPK and NPKM fertilization. The results showed that the NPKM fertilization of the millet field had a maximal yield of 3617 kg ha-1 among the six different treatments. The abundances of the Actinobacteria and Bacteroidetes phyla, especially the Devosia, Mycobacterium, Opitutus and Chitinophaga genera, were higher in NPKM than those in the other samples. Redundancy analysis showed that the soil organic matter (SOM), available phosphorus (AP), and urease (UR) activity were significantly correlated with bacterial communities, while SOM and AP were strongly correlated with soil enzyme activities. Pearson's correlation showed that the available nitrogen was strongly correlated with Devosia and Mycobacterium, and SOM was strongly correlated with Opitutus and Chitinophaga. Besides, catalase was significantly related to Iamia, the UR was significantly related to Devosia, phosphatase was significantly related to Luteimonas and Chitinophaga. Based on the soil quality and millet yield, NPKM treatment was a better choice for the millet field fertilization practices. These findings provide a better understanding of the importance of fertilization in influencing millet yield, soil fertility and microbial diversity, and they lead to a choice of scientific fertilization practices for sustainable development of the agroecosystem.


Assuntos
Ativação Enzimática/efeitos dos fármacos , Esterco , Consórcios Microbianos/efeitos dos fármacos , Milhetes/microbiologia , Minerais/farmacologia , Rizosfera , Microbiologia do Solo , Agricultura , Bactérias/classificação , Bactérias/efeitos dos fármacos , Bactérias/enzimologia , Bactérias/genética , Biodiversidade , Biomassa , China , Grão Comestível/microbiologia , Fertilizantes , Sequenciamento de Nucleotídeos em Larga Escala , Consórcios Microbianos/genética , Minerais/análise , Nitrogênio/análise , Nitrogênio/farmacologia , Fosfatos , Potássio , RNA Ribossômico 16S/genética , Solo/química
12.
Ecotoxicology ; 26(9): 1181-1187, 2017 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-28819808

RESUMO

Sulfur dioxide (SO2) is a common air pollutant that has adverse effects on plants. MicroRNAs (miRNAs) are small noncoding RNA that play critical roles in plant development and stress response. In this study, we found that two miRNAs, miR398 and miR395, were differentially expressed in Arabidopsis shoots under SO2 stress. The expression of miR398 was down-regulated, and the transcript levels of its target genes, Cu/Zn superoxide dismutases (CSD1 and CSD2), were increased during SO2 exposure. The activity of superoxide dismutase (SOD), one of the major antioxidant enzymes, was enhanced with the increase in the CSD transcript level, suggesting an important role of miR398 in response to SO2-induced oxidative stress. Meanwhile, the expression of miR395 was increased, and the transcript levels of its target genes, ATP sulfurylases (APS3 and APS4) and a low-affinity sulfate transporter (SULTR2;1), were decreased in Arabidopsis shoots, showing that miR395 played important roles in the regulation of sulfate assimilation and translocation during SO2 exposure. The content of glutathione (GSH), an important sulfur-containing antioxidant, was enhanced with the changes in sulfur metabolism in Arabidopsis shoots under SO2 stress. These results showed that both miR398 and miR395 were involved in protecting plants from oxidative damage during SO2 exposure. Many stress-responsive cis-elements were found in the promoter regions of MIR398 and MIR395, suggesting that these miRNAs might respond to various environmental conditions, including SO2 stress. Overall, our study provides an insight into the regulatory roles of miRNAs in response to SO2 stress in plants, and highlights the molecular mechanisms of plant adaptation to environmental stress.


Assuntos
Arabidopsis/fisiologia , Substâncias Perigosas/toxicidade , MicroRNAs , Estresse Fisiológico/genética , Dióxido de Enxofre/toxicidade , Arabidopsis/genética , Sulfato Adenililtransferase , Superóxido Dismutase/metabolismo
13.
Environ Sci Pollut Res Int ; 24(10): 9437-9446, 2017 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-28236197

RESUMO

NO and H2O2 have been implicated as important signals in biotic and abiotic stress responses of plants to the environment. Previously, we have shown that SO2 exposure increased the levels of NO and H2O2 in plant cells. We hypothesize that, as signaling molecules, NO and H2O2 mediate SO2-caused toxicity. In this paper, we show that SO2 hydrates caused guard cell death in a concentration-dependent manner in the concentration range of 0.25 to 6 mmol L-1, which was associated with elevation of intracellular NO, H2O2, and Ca2+ levels in Vicia faba guard cells. NO donor SNP enhanced SO2 toxicity, while NO scavenger c-PTIO and NO synthesis inhibitors L-NAME and tungstate significantly prevented SO2 toxicity. ROS scavenger ascorbic acid (AsA) and catalase (CAT), Ca2+ chelating agent EGTA, and Ca2+ channel inhibitor LaCl3 also markedly blocked SO2 toxicity. In addition, both c-PTIO and AsA could completely block SO2-induced elevation of intracellular Ca2+ level. Moreover, c-PTIO efficiently blocked SO2-induced H2O2 elevation, and AsA significantly blocked SO2-induced NO elevation. These results indicate that extra NO and H2O2 are produced and accumulated in SO2-treated guard cells, which further activate Ca2+ signaling to mediate SO2 toxicity. Our findings suggest that both NO and H2O2 contribute to SO2 toxicity via Ca2+ signaling.


Assuntos
Peróxido de Hidrogênio/metabolismo , Vicia faba/metabolismo , Catalase/metabolismo , NG-Nitroarginina Metil Éster , Transdução de Sinais/efeitos dos fármacos
14.
Can J Microbiol ; 63(2): 153-159, 2017 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-27995805

RESUMO

Cadmium (Cd) is one of the most toxic heavy metals. It is of great environmental concern and its toxicity has been investigated in a variety of cells. In this study, we elucidated the toxic effects of Cd in cells of yeast (Saccharomyces cerevisiae). Our results showed that Cd2+ (0.05-5.0 mmol·L-1) significantly inhibited yeast cell growth, and the inhibitory effect was positively correlated with Cd2+ concentrations. Cd2+ caused loss of yeast cell viability in a concentration- and duration-dependent manner. Intracellular reactive oxygen species (ROS) and Ca2+ levels increased in yeast cells after exposure to 5.0 mmol·L-1 Cd for 6 h. Cd2+-caused cell viability loss was blocked by antioxidants (0.5 mmol·L-1 ascorbic acid or 500 U·mL-1 catalase) or Ca2+ antagonists (0.5 mmol·L-1 ethylene glycol tetraacetic acid or 0.5 mmol·L-1 LaCl3). Moreover, a collapse of mitochondrial membrane potential (ΔΨm) was observed in Cd2+-treated yeast cells. These results indicate that Cd-induced yeast cell killing was associated with the elevation of intracellular ROS and Ca2+ levels and also the loss of ΔΨm.


Assuntos
Cádmio/toxicidade , Espécies Reativas de Oxigênio/metabolismo , Saccharomyces cerevisiae/efeitos dos fármacos , Antioxidantes/farmacologia , Catalase/farmacologia , Saccharomyces cerevisiae/metabolismo
15.
J Hazard Mater ; 316: 178-85, 2016 10 05.
Artigo em Inglês | MEDLINE | ID: mdl-27232729

RESUMO

Sulfur dioxide (SO2) is a major air pollutant and has significant impacts on plants. MicroRNAs (miRNAs) are a class of gene expression regulators that play important roles in response to environmental stresses. In this study, deep sequencing was used for genome-wide identification of miRNAs and their expression profiles in response to SO2 stress in Arabidopsis thaliana shoots. A total of 27 conserved miRNAs and 5 novel miRNAs were found to be differentially expressed under SO2 stress. qRT-PCR analysis showed mostly negative correlation between miRNA accumulation and target gene mRNA abundance, suggesting regulatory roles of these miRNAs during SO2 exposure. The target genes of SO2-responsive miRNAs encode transcription factors and proteins that regulate auxin signaling and stress response, and the miRNAs-mediated suppression of these genes could improve plant resistance to SO2 stress. Promoter sequence analysis of genes encoding SO2-responsive miRNAs showed that stress-responsive and phytohormone-related cis-regulatory elements occurred frequently, providing additional evidence of the involvement of miRNAs in adaption to SO2 stress. This study represents a comprehensive expression profiling of SO2-responsive miRNAs in Arabidopsis and broads our perspective on the ubiquitous regulatory roles of miRNAs under stress conditions.


Assuntos
Arabidopsis/genética , Regulação da Expressão Gênica de Plantas , Sequenciamento de Nucleotídeos em Larga Escala , MicroRNAs/genética , RNA de Plantas/genética , Dióxido de Enxofre/química , Biologia Computacional , Perfilação da Expressão Gênica , Genes de Plantas , RNA Mensageiro/genética , Estresse Fisiológico , Transcriptoma
16.
Zhongguo Zhong Yao Za Zhi ; 41(16): 2968-2974, 2016 Aug.
Artigo em Chinês | MEDLINE | ID: mdl-28920333

RESUMO

Ellagitannins is a kind of phenolic compounds with many biological activities. Recent studies have found that the effective ingredients of these compounds have close relationship with their colon-derived bacteria metabolites, that is urolithins. The objective of this study was to review the structure characteristics, types and distribution of urolithins, improvement in diseases related to prostate, breast and colon, as well as anti-cancer, anti-oxidation, anti-inflammation and other biological activities. The present review will lay the foundation for development and utilization of urolithins.


Assuntos
Cumarínicos/química , Taninos Hidrolisáveis/química , Neoplasias da Mama , Neoplasias do Colo , Feminino , Humanos , Inflamação , Intestinos/microbiologia , Masculino , Neoplasias da Próstata
17.
Phytother Res ; 29(3): 415-22, 2015 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-25572695

RESUMO

miRNAs and their validated miRNA targets appear as novel effectors in biological activities of plant polyphenols; however, limited information is available on miR-34a mediated cytotoxicity of pomegranate rind polyphenols in cancer cell lines. For this purpose, cell viability assay, Realtime quantitative PCR for mRNA quantification, western blot for essential protein expression, p53 silencing by shRNA and miR-34a knockdown were performed in the present study. EJ cell treatment with 100 µg (GAE)/mL PRE for 48 h evoked poor cell viability and caspase-dependent pro-apoptosis appearance. PRE also elevated p53 protein and triggered miR-34a expression. The c-Myc and CD44 were confirmed as direct targets of miR-34a in EJ cell apoptosis induced by PRE. Our results provide sufficient evidence that polyphenols in PRE can be potential molecular clusters to suppress bladder cancer cell EJ proliferation via p53/miR-34a axis.


Assuntos
Antineoplásicos Fitogênicos/farmacologia , MicroRNAs/metabolismo , Polifenóis/farmacologia , Punicaceae/química , Proteína Supressora de Tumor p53/metabolismo , Neoplasias da Bexiga Urinária/metabolismo , Animais , Apoptose/efeitos dos fármacos , Linhagem Celular Tumoral/efeitos dos fármacos , Proliferação de Células/efeitos dos fármacos , Sobrevivência Celular , Células Epiteliais/efeitos dos fármacos , Frutas/química , Regulação Neoplásica da Expressão Gênica , Inativação Gênica , Humanos , Receptores de Hialuronatos/metabolismo , Masculino , Camundongos Nus , MicroRNAs/genética , Proteínas Proto-Oncogênicas c-myc/metabolismo , RNA Interferente Pequeno , Ratos , Proteína Supressora de Tumor p53/genética , Neoplasias da Bexiga Urinária/patologia
18.
Mol Genet Genomics ; 289(5): 989-99, 2014 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-24889700

RESUMO

Sulfur dioxide (SO2) supplies the basic sulfur element to promote plant growth, yet at the same time it is a harmful air pollutant. Currently, the mechanisms of plant adaptation to SO2 stress are largely unknown. Pathways of SO2 metabolism, a range of networks of interacting regulatory signals and defense mechanisms triggered in resistance to SO2 stress, have not yet been clarified. We performed transcriptome analysis of Arabidopsis plants fumigated with 30 mg m(-3) SO2 for 72 h and untreated controls using microarrays. This identified 2,780 significantly up- or down-regulated genes in plants response to SO2 stress, indicating a possible genome-scale reprogramming of the transcriptome. Significant changes in the transcript abundance of genes that participated in SO2 metabolic pathways indicated that numerous sulfites were involved in sulfur assimilatory pathways directly and away from sulfite oxidative pathways. Furthermore, the up-regulation of components involved in reactive oxygen species generating and scavenging pathways demonstrated altered redox homeostasis. Transcripts encoding key components in nitric oxide biosynthesis pathways were simultaneously up-regulated by SO2 exposure. In addition, transcripts associated with putative biotic stress were also up-regulated. Therefore, SO2 evokes a comprehensive reprogramming of metabolic pathways, consistent with up-regulation of transcripts involved in tolerance and defense mechanisms, in Arabidopsis.


Assuntos
Poluentes Atmosféricos/farmacologia , Arabidopsis/genética , Dióxido de Enxofre/farmacologia , Transcriptoma , Adaptação Fisiológica , Arabidopsis/efeitos dos fármacos , Arabidopsis/metabolismo , Proteínas de Arabidopsis/genética , Proteínas de Arabidopsis/metabolismo , Metabolismo Energético/efeitos dos fármacos , Fumigação , Perfilação da Expressão Gênica , Regulação da Expressão Gênica de Plantas/efeitos dos fármacos , Genoma de Planta , Homeostase , Redes e Vias Metabólicas/genética , Oxirredução , Estresse Fisiológico
19.
FEMS Microbiol Lett ; 343(1): 57-63, 2013 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-23510033

RESUMO

Arsenic is a toxic metalloid that is widely distributed in the environment, and its toxicity has been demonstrated in several models. However, the mechanism of arsenic toxicity still remains unclear. In this study, the toxic effects of sodium arsenite (1-7 mM) on yeast cells were investigated. The experimental results showed that sodium arsenite inhibited yeast cell growth, and the inhibitory effect of cell growth (OD600 nm values) was positively correlated with arsenite concentrations. Sodium arsenite caused loss of cell viability in a concentration- and duration-dependent manner in yeast cells. However, arsenite-caused cell viability loss was blocked by either antioxidants (200 U mL(-1) CAT and 0.5 mM AsA) or Ca(2+) antagonists (0.5 mM LaCl3 and 0.5 mM EGTA). We also found intracellular reactive oxygen species (ROS) and Ca(2+) levels increased significantly in yeast cells after exposure to 3 mM and 7 mM sodium arsenite for 6 h compared with the control. These results indicated that high concentrations of arsenite-induced yeast cell killing was associated with elevated levels of intracellular ROS and Ca(2+).


Assuntos
Arsenitos/toxicidade , Cálcio/metabolismo , Viabilidade Microbiana/efeitos dos fármacos , Espécies Reativas de Oxigênio/metabolismo , Saccharomyces cerevisiae/efeitos dos fármacos , Compostos de Sódio/toxicidade , Arsenitos/metabolismo , Cátions Bivalentes/metabolismo , Citosol/química , Compostos de Sódio/metabolismo
20.
Plant Physiol Biochem ; 58: 46-53, 2012 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-22771435

RESUMO

Sulfur dioxide (SO(2)) is one of the most common and harmful air pollutants. To analyze antioxidant response of plants to SO(2) stress, we investigated the reactive oxygen species (ROS) levels, transcript alterations and antioxidant enzyme activities in Arabidopsis thaliana (Col-0) exposed to 0, 2.5, 10 and 30 mg m(-3) of SO(2). The results showed that both superoxide radical (O(2)(-⋅)) generation rate and hydrogen peroxide (H(2)O(2)) content increased in SO(2)-treated Arabidopsis shoots. GeneChip and RT-PCR analysis revealed that transcript levels of peroxidase (POD), glutathione peroxidase (GPX) and superoxide dismutase (SOD) genes enhanced after exposure to 30 mg m(-3) SO(2) for 72 h. The content of glutathione and activities of SOD, POD and GPX increased significantly during 72 h of SO(2) exposure. However, catalases (CAT) activity changed slightly under SO(2) stress. Furthermore, the results of in-gel enzyme assays indicated that SOD (FeSOD and Cu/ZnSOD) and POD isoforms increased after exposure to SO(2) for 72 h, whereas two CAT isoforms (CAT2 and CAT3) declined. Malondialdehyde content kept at a low level within 72 h of SO(2) exposure, but increased significantly after exposure to 30 mg m(-3) SO(2) for 120 h along with decrease in the level of ROS and activities of SOD and GPX. Our results indicated that increased ROS may act as a signal to induce defense response to SO(2) stress. Antioxidant status plays an important role in plant protection against SO(2)-caused oxidative stress, though the defense capacity cannot sufficiently alleviate oxidative damage occurring under prolonged exposure to higher concentrations of SO(2).


Assuntos
Poluentes Atmosféricos/farmacologia , Antioxidantes/metabolismo , Arabidopsis/efeitos dos fármacos , Expressão Gênica/efeitos dos fármacos , Estresse Oxidativo/efeitos dos fármacos , Espécies Reativas de Oxigênio/metabolismo , Dióxido de Enxofre/farmacologia , Arabidopsis/genética , Arabidopsis/metabolismo , Proteínas de Arabidopsis/metabolismo , Enzimas/genética , Enzimas/metabolismo , Genes de Plantas , Malondialdeído/metabolismo , Isoformas de Proteínas , Transdução de Sinais
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