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2.
Water Sci Technol ; 82(7): 1327-1338, 2020 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-33079713

RESUMO

Advanced oxidative processes (AOP) have been consolidated as an efficient treatment technique to degrade persistent contaminants. In addition to them, biosorption also emerges as a technique capable of removing both pollutants and intermediate products generated by other treatments such as AOP. Thus, this work evaluated the degradation and removal of the mixture of dyes Direct Red 23 and Direct Red 227 in aqueous solution (50 mg·L-1 of each). Preliminary tests showed that the photo-Fenton system under sunlight radiation was the most efficient, reaching a degradation ≥93%. For the adsorptive process using chicken eggshell, preliminary tests indicated that the ideal dosage of adsorbent was 8.0 g·L-1. For this process, a factorial design indicated the best working conditions, which demonstrated from the system adjusted well to the Elovich (kinetic) model and to the Freundlich and Sips models (equilibrium). When associating the two processes, AOP followed by adsorption achieved a total degradation/removal of ≈98% (for all λ) in a time of 60 min. Thus, the feasibility of the combined treatment is indicated.


Assuntos
Corantes , Têxteis , Adsorção , Animais , Concentração de Íons de Hidrogênio , Estresse Oxidativo
3.
Eur Respir Rev ; 29(157)2020 Sep 30.
Artigo em Inglês | MEDLINE | ID: mdl-33004527

RESUMO

The respiratory tract and its resident immune cells face daily exposure to stress, both from without and from within. Inhaled pathogens, including severe acute respiratory syndrome coronavirus 2, and toxins from pollution trigger a cellular defence system that reduces protein synthesis to minimise viral replication or the accumulation of misfolded proteins. Simultaneously, a gene expression programme enhances antioxidant and protein folding machineries in the lung. Four kinases (PERK, PKR, GCN2 and HRI) sense a diverse range of stresses to trigger this "integrated stress response". Here we review recent advances identifying the integrated stress response as a critical pathway in the pathogenesis of pulmonary diseases, including pneumonias, thoracic malignancy, pulmonary fibrosis and pulmonary hypertension. Understanding the integrated stress response provides novel targets for the development of therapies.


Assuntos
Inflamação/metabolismo , Pneumopatias/metabolismo , Estresse Oxidativo/fisiologia , Biomarcadores/metabolismo , Humanos
4.
Beijing Da Xue Xue Bao Yi Xue Ban ; 52(5): 821-827, 2020 Oct 18.
Artigo em Chinês | MEDLINE | ID: mdl-33047714

RESUMO

OBJECTIVE: To evaluate the sub-acute oral effect of titanium dioxide (TiO2) nanoparticles on the oxidation/antioxidation biomarkers and inflammatory cytokines in blood, liver, intestine, and colon in rats. METHODS: Twenty four 4-week-old clean-grade Sprague Dawley (SD) rats were randomly devided into 4 groups by body weight (n=6, control, low, middle, and high), in which the rats were orally exposed to TiO2 nanoparticles at doses of 0, 2, 10 and 50 mg/kg body weight/day for 28 consecutive days separately. Food intake, body weight and abnormal behaviors during the experiment were recorded. The rats were euthanized on the 29th day. The blood was collected via abdominal aortic method and centrifuged to collect the serum. Tissues from liver, intestine and colon were collected and homogenated. Then enzyme-linked immunosorbent assay (ELISA) and microwell plate methods were used to detect oxidation/antioxidation biomarkers including superoxide dismutase (SOD), glutathione (GSH), glutathione peroxidase (GSH-Px), total mercapto (T-SH), glutathione disulfide (GSSG), malomdialdehvde (MDA) and inflammatory cytokines including interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) in the serum, liver, intestine and colon in the rats. RESULTS: Compared with the control group, no significant differences in body weight, food intake and organ coefficients were observed in all the three groups after TiO2 gavage. No significant changes in GSH, GSH-Px, T-SH, and IL-6 were observed. Compared with the control group, significant increase of SOD activity in serum in high dose group, signi-ficant increase of GSSG concentration in intestine in middle and high dose group and significant increase of MDA concentration in liver in low and high dose group were observed. Compared with the control group, a significant increase of TNF-α in liver in middle and high dose group was observed. CONCLUSION: TiO2 nanoparticle can increase antioxidant enzymes activities in blood, increase oxidative biomarkers in liver and intestine, increase inflammatory cytokines in liver in rats after a 28-day sub-acute orally administration. Among blood, liver, intestine, and colon, liver is most sensitive to the toxicity induced by TiO2 nanoparticles, followed by intestine, blood, and colon in sequence.


Assuntos
Antioxidantes , Nanopartículas , Animais , Biomarcadores , Citocinas , Estresse Oxidativo , Ratos , Ratos Sprague-Dawley , Titânio
5.
Annu Int Conf IEEE Eng Med Biol Soc ; 2020: 2266-2269, 2020 07.
Artigo em Inglês | MEDLINE | ID: mdl-33018459

RESUMO

This paper describes a method for deciphering major drivers of bacterial stress response using an empirically informed computational approach. We develop a working model of iron flux regulation and concomitant oxidative stress response in Escherichia coli. The integrated model is used to investigate the temporal effects of iron and hydrogen peroxide stress on bacterial growth and metabolism. We employ a sensitivity analysis platform and, using various measures, probe for major mechanistic drivers of the bacterial response to iron stress.


Assuntos
Peróxido de Hidrogênio , Ferro , Bactérias , Oxirredução , Estresse Oxidativo
6.
Biochemistry (Mosc) ; 85(7): 833-837, 2020 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-33040727

RESUMO

Nrf2 is a key transcription factor responsible for antioxidant defense in many tissues and cells, including alveolar epithelium, endothelium, and macrophages. Furthermore, Nrf2 functions as a transcriptional repressor that inhibits expression of the inflammatory cytokines in macrophages. Critically ill patients with COVID-19 infection often present signs of high oxidative stress and systemic inflammation - the leading causes of mortality. This article suggests rationale for the use of Nrf2 inducers to prevent development of an excessive inflammatory response in COVID-19 patients.


Assuntos
Betacoronavirus , Infecções por Coronavirus/tratamento farmacológico , Infecções por Coronavirus/metabolismo , Citocinas/antagonistas & inibidores , Citocinas/metabolismo , Terapia de Alvo Molecular/métodos , Fator 2 Relacionado a NF-E2/metabolismo , Pneumonia Viral/tratamento farmacológico , Pneumonia Viral/metabolismo , Animais , Antioxidantes/farmacologia , Antioxidantes/uso terapêutico , Catequina/análogos & derivados , Catequina/farmacologia , Catequina/uso terapêutico , Infecções por Coronavirus/virologia , Fumarato de Dimetilo/farmacologia , Fumarato de Dimetilo/uso terapêutico , Feminino , Humanos , Imunossupressores/farmacologia , Imunossupressores/uso terapêutico , Inflamação/metabolismo , Isotiocianatos/farmacologia , Isotiocianatos/uso terapêutico , Masculino , Camundongos , Estresse Oxidativo/efeitos dos fármacos , Pandemias , Pneumonia Viral/virologia , Síndrome do Desconforto Respiratório do Adulto/tratamento farmacológico , Síndrome do Desconforto Respiratório do Adulto/metabolismo , Síndrome do Desconforto Respiratório do Adulto/virologia , Resveratrol/farmacologia , Resveratrol/uso terapêutico , Transdução de Sinais/efeitos dos fármacos , Tiossulfatos/farmacologia , Tiossulfatos/uso terapêutico
7.
Med Hypotheses ; 143: 110185, 2020 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-33017914

RESUMO

COVID-19 pandemic is spreading rapidly worldwide, and drug selection can affect the morbidity and mortality of the disease positively or negatively. Alpha-lipoic acid (ALA) is a potent antioxidant and reduces oxidative stress and inhibits activation of nuclear factor-kappa B (NF-kB). ALA reduces ADAM17 activity and ACE2 upregulation. ALA is known to have antiviral effects against some viruses. ALA may show antiviral effect by reducing NF-kB activation and alleviating redox reactions. ALA increases the intracellular glutathione strengthens the human host defense. ALA activates ATP dependent K+ channels (Na+, K+-ATPase). Increased K+ in the cell raises the intracellular pH. As the intracellular pH increases, the entry of the virus into the cell decreases. ALA can increase human host defense against SARS-CoV-2 by increasing intracellular pH. ALA treatment increases antioxidant levels and reduces oxidative stress. Thus, ALA may strengthen the human host defense against SARS-CoV-2 and can play a vital role in the treatment of patients with critically ill COVID-19. It can prevent cell damage by decreasing lactate production in patients with COVID-19. Using ALA with insulin in patients with diabetes can show a synergistic effect against SARS-CoV-2. We think ALA treatment will be beneficial against COVID-19 in patients with diabetes.


Assuntos
Proteína ADAM17/metabolismo , Infecções por Coronavirus/prevenção & controle , Complicações do Diabetes/prevenção & controle , NF-kappa B/metabolismo , Pandemias/prevenção & controle , Peptidil Dipeptidase A/metabolismo , Pneumonia Viral/prevenção & controle , Ácido Tióctico/uso terapêutico , Antioxidantes/uso terapêutico , Betacoronavirus , Infecções por Coronavirus/complicações , Complicações do Diabetes/virologia , Diabetes Mellitus/tratamento farmacológico , Humanos , Concentração de Íons de Hidrogênio , Insulina/metabolismo , Oxirredução , Estresse Oxidativo , Pneumonia Viral/complicações
8.
Life Sci ; 259: 118379, 2020 Oct 15.
Artigo em Inglês | MEDLINE | ID: mdl-32890604

RESUMO

With the increasing application of medical imaging contrast materials, contrast-induced nephropathy has become one of the leading causes of iatrogenic renal insufficiency. The underlying mechanism is associated with renal medullary hypoxia, direct toxicity of contrast agents, oxidative stress, apoptosis, immune/inflammation and epigenetic regulation in contrast-induced nephropathy. Up to date, there is no effective therapy for contrast-induced nephropathy, and thus risk predication and effective preventive strategies are keys to reduce the occurrence of contrast-induced nephropathy. It was found that the proper use of contrast medium, personalized hydration, and high-dose statins may reduce the occurrence of contrast-induced nephropathy, while antioxidants have not shown significant therapeutic benefits. Additionally, the role of remote ischemia preconditioning and vasodilators in the prevention of contrast-induced nephropathy needs further study. This review aims to discuss the incidence, pathogenesis, risk prediction, and preventive strategies for contrast-induced nephropathy.


Assuntos
Meios de Contraste/efeitos adversos , Nefropatias/induzido quimicamente , Humanos , Rim/efeitos dos fármacos , Nefropatias/prevenção & controle , Estresse Oxidativo/efeitos dos fármacos
9.
Life Sci ; 259: 118382, 2020 Oct 15.
Artigo em Inglês | MEDLINE | ID: mdl-32898532

RESUMO

AIM: Vancomycin (VCM) is a glycopeptide antibiotic widely used to treat serious infections caused by methicillin-resistant Staphylococcus aureus and has been associated with some severe side effects such as hepatotoxicity and nephrotoxicity. However, the underlying mechanism of VCM-induced hepatotoxicity is not yet fully understood. Therefore, the current study was designed to evaluate the protective effects of zingerone (Zin) against VCM-induced hepatotoxicity in rats. MATERIALS AND METHODS: VCM was intraperitoneally administered at a dose of 200 mg/kg body weight (b.w.) for 7 days alone and in combination with the orally administered Zin (25 and 50 mg/kg b.w). KEY FINDINGS: Zin treatment significantly improved VCM-induced hepatic lipid peroxidation, glutathione depletion, reduced antioxidant enzyme (superoxide dismutase, catalase and glutathione peroxidase) activities and liver function markers (aspartate aminotransferase, alkaline phosphatase and alanine aminotransferase). Histopathological integrity and immunohistochemical expression of 8-hydroxy-2'-deoxyguanosine (8-OHdG) in the VCM-induced liver tissue were ameliorated after Zin administration. In addition, Zin reversed the changes in levels and/or activities of inflammatory and apoptotic parameters such as nuclear factor kappa B (NF-κB), tumor necrosis factor-α (TNF-α), interleukin-1ß (IL-1ß), inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), p53, cysteine aspartate specific protease-3 (caspase-3), cysteine aspartate specific protease-8 (caspase-8), cytochrome c, Bcl-2 associated X protein (Bax) and B-cell lymphoma-2 (Bcl-2) in the VCM-induced hepatotoxicity. SIGNIFICANCE: Collectively, these results reveal probable ameliorative role of Zin against VCM-induced hepatotoxicity.


Assuntos
Apoptose/efeitos dos fármacos , Doença Hepática Induzida por Substâncias e Drogas/tratamento farmacológico , Guaiacol/análogos & derivados , Inflamação/tratamento farmacológico , Estresse Oxidativo/efeitos dos fármacos , Vancomicina/toxicidade , Animais , Western Blotting , Ciclo-Oxigenase 2/metabolismo , Guaiacol/uso terapêutico , Interleucina-1beta/metabolismo , Peroxidação de Lipídeos/efeitos dos fármacos , Fígado/efeitos dos fármacos , Fígado/metabolismo , Masculino , NF-kappa B/metabolismo , Óxido Nítrico Sintase Tipo II/metabolismo , Ratos , Ratos Sprague-Dawley , Fator de Necrose Tumoral alfa/metabolismo
10.
Aquat Toxicol ; 227: 105625, 2020 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-32927179

RESUMO

Here we report the molecular networks associated with the mucosal and systemic responses to peracetic acid (PAA), a candidate oxidative chemotherapeutic in Atlantic salmon (Salmo salar). Smolts were exposed to different therapeutic doses (0, 0.6 and 2.4 mg/L) of PAA for 5 min, followed by a re-exposure to the same concentrations for 30 min 2 weeks later. PAA-exposed groups have higher external welfare score alterations, especially 2 weeks after the re-exposure. Cases of fin damage and scale loss were prevalent in the PAA-exposed groups. Transcriptomic profiling of mucosal tissues revealed that the skin had 12.5 % more differentially regulated genes (DEGs) than the gills following PAA exposure. The largest cluster of DEGs, both in the skin and gills, were involved in tissue extracellular matrix and metabolism. There were 22 DEGs common to both mucosal tissues, which were represented primarily by genes involved in the biophysical integrity of the mucosal barrier, including cadherin, collagen I α 2 chain, mucin-2 and spondin 1a. The absence of significant clustering in the plasma metabolomes amongst the three treatment groups indicates that PAA treatment did not induce any global metabolomic disturbances. Nonetheless, five metabolites with known functions during oxidative stress were remarkably affected by PAA treatments such as citrulline, histidine, tryptophan, methionine and trans-4-hydroxyproline. Collectively, these results indicate that salmon were able to mount mucosal and systemic adaptive responses to therapeutic doses of PAA and that the molecules identified are potential markers for assessing the health and welfare consequences of oxidant exposure.


Assuntos
Metaboloma , Transcriptoma , Poluentes Químicos da Água/toxicidade , Animais , Biomarcadores/metabolismo , Doenças dos Peixes/genética , Perfilação da Expressão Gênica , Brânquias/efeitos dos fármacos , Membrana Mucosa/metabolismo , Oxidantes/metabolismo , Estresse Oxidativo , Salmo salar/metabolismo
11.
Clinics (Sao Paulo) ; 75: e1865, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32935825

RESUMO

OBJECTIVES: Hypoxia leads to endothelial cell inflammation, apoptosis, and damage, which plays an important role in the complications associated with ischemic cardiovascular disease. As an oxidoreductase, p66Shc plays an important role in the regulation of reactive oxygen species (ROS) production and apoptosis. Ketamine is widely used in clinics. This study was designed to assess the potential protective effect of ketamine against hypoxia-induced injury in human umbilical vein endothelial cells (HUVECs). Moreover, we explored the potential mechanism by which ketamine protected against hypoxia-induced endothelial injury. METHODS: The protective effects of ketamine against hypoxia-induced injury was assessed using cell viability and adhesion assays, quantitative polymerase chain reaction, and western blotting. RESULTS: Our data showed that hypoxia reduced HUVEC viability, increased the adhesion between HUVECs and monocytes, and upregulated the expression of endothelial adhesion molecules at the protein and mRNA levels. Moreover, hypoxia increased ROS accumulation and upregulated p66Shc expression. Furthermore, hypoxia downregulated sirt1 expression in HUVECs. Alternatively, ketamine was shown to reverse the hypoxia-mediated reduction of cell viability and increase in the adhesion between HUVECs and monocytes, ameliorate hypoxia-induced ROS accumulation, and suppress p66Shc expression. Moreover, EX527, a sirt1 inhibitor, reversed the protective effects of ketamine against the hypoxia-mediated reduction of cell viability and increase in adhesion between HUVECs and monocytes. CONCLUSION: Ketamine reduces hypoxia-induced p66Shc expression and attenuates ROS accumulation via upregulating sirt1 in HUVECs, thus attenuating hypoxia-induced endothelial cell inflammation and apoptosis.


Assuntos
Apoptose/efeitos dos fármacos , Células Endoteliais da Veia Umbilical Humana/efeitos dos fármacos , Hipóxia , Ketamina/farmacologia , Espécies Reativas de Oxigênio/metabolismo , Sobrevivência Celular , Células Endoteliais da Veia Umbilical Humana/metabolismo , Humanos , Estresse Oxidativo , Proteína 1 de Transformação que Contém Domínio 2 de Homologia de Src , Veias Umbilicais
12.
Nat Commun ; 11(1): 4870, 2020 09 25.
Artigo em Inglês | MEDLINE | ID: mdl-32978384

RESUMO

Little is known about the physiology of latent Mycobacterium tuberculosis infection. We studied the mutational rates of 24 index tuberculosis (TB) cases and their latently infected household contacts who developed active TB up to 5.25 years later, as an indication of bacterial physiological state and possible generation times during latent TB infection in humans. Here we report that the rate of new mutations in the M. tuberculosis genome decline dramatically after two years of latent infection (two-sided p < 0.001, assuming an 18 h generation time equal to log phase M. tuberculosis, with latency period modeled as a continuous variable). Alternatively, assuming a fixed mutation rate, the generation time increases over the latency duration. Mutations indicative of oxidative stress do not increase with increasing latency duration suggesting a lack of host or bacterial derived mutational stress. These results suggest that M. tuberculosis enters a quiescent state during latency, decreasing the risk for mutational drug resistance and increasing generation time, but potentially increasing bacterial tolerance to drugs that target actively growing bacteria.


Assuntos
Tuberculose Latente/microbiologia , Taxa de Mutação , Mycobacterium tuberculosis/genética , Tuberculose/microbiologia , Adulto , Brasil , DNA Bacteriano/isolamento & purificação , Feminino , Genoma Bacteriano , Humanos , Masculino , Mutação , Mycobacterium tuberculosis/patogenicidade , Estresse Oxidativo , Filogenia , Polimorfismo de Nucleotídeo Único , Fatores de Tempo , Adulto Jovem
13.
Chemosphere ; 258: 127385, 2020 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-32947675

RESUMO

2,2,4,4-tetrabromodiphenyl ether (BDE-47) has received considerable attention because of its high detection level in biological samples and potential developmental toxicity. Here, using zebrafish (Danio rerio) as the experimental animal, we investigated developmental effects of BDE-47 and explored the potential mechanism. Zebrafish embryos at 4 h post-fertilization (hpf) were exposed to 0.312, 0.625 and 1.25 mg/L BDE-47 to 74-120 hpf. We found that BDE-47 instigated a dose-related developmental toxicity, evidenced by reduced embryonic survival and hatching rate, shortened body length and increased aberration rate. Meanwhile, higher doses of BDE-47 reduced mitochondrial membrane potential and ATP production but increased apoptosis in zebrafish embryos. Expression of genes involved in mitochondrial oxidative phosphorylation (OXPHOS) (ndufb8, sdha, uqcrc1, cox5ab and atp5fal) were negatively related to BDE-47 doses in zebrafish embryos. Moreover, exposure to BDE-47 at 0.625 or 1.25 mg/L impaired mitochondrial biogenesis and mitochondrial dynamics. Our data further showed that BDE- 47 exposure induced excessive reactive oxygen species (ROS) and oxidative stress, which was accompanied by the activation of c-Jun N-terminal Kinase (JNK). Antioxidant NAC and JNK inhibition could mitigate apoptosis in embryos and improve embryonic development in BDE-47-treated zebrafish, suggesting the involvement of ROS/JNK pathway in embryonic developmental changes induced by BDE-47. Altogether, our data suggest here that developmental toxicity of BDE-47 may be associated with mitochondrial ROS-mediated JNK signaling in zebrafish embryo.


Assuntos
Éteres Difenil Halogenados/toxicidade , Poluentes Químicos da Água/toxicidade , Animais , Antioxidantes/metabolismo , Apoptose/efeitos dos fármacos , Embrião não Mamífero/efeitos dos fármacos , Desenvolvimento Embrionário/efeitos dos fármacos , Sistema de Sinalização das MAP Quinases , Mitocôndrias/metabolismo , Estresse Oxidativo/efeitos dos fármacos , Espécies Reativas de Oxigênio/metabolismo , Peixe-Zebra/metabolismo
14.
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
15.
Pestic Biochem Physiol ; 170: 104671, 2020 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-32980069

RESUMO

TEB belongs to the family of triazole fungicides and it is used to protect agricultural crop plants from fungal pathogens. The information regarding its cardiotoxic effects through different pathways particularly by perturbing the oxidative balance and causing damage to the myocardium is still limited. In the present study, oxidative and histopathologic damages caused by TEB in the cardiac tissue of male adult rats, were evaluated. Rats were exposed orally to TEB at 0.9, 9, 27 and 45 mg/kg b.w. for 28 days. Results showed that following TEB treatment malondialdehyde (MDA), protein carbonyl (PC), advanced oxidation protein product (AOPP), antioxidant enzyme activities (GPx and GR) and GSSG levels increased, while GSH levels and thus the GSH/GSSG ratio decreased. Superoxide dismutase (SOD) and catalase (CAT) initially increased at the doses of 0.9, 9 and 27 mg/kg b.w. and then decreased at the dose of 45 mg/kg b.w. Moreover, western blot analysis showed that TEB increased SOD1, CAT and HSP70 protein levels after 24 h. Furthermore, TEB induced various histological changes in the myocardium, including leucocytic infiltration, hemorrhage congestion of cardiac blood vessels and cytoplasmic vacuolization. Therefore, our investigation revealed, that TEB exhibits cardiotoxic effects by changing oxidative balance and damaging the cardiac tissue.


Assuntos
Glutationa , Estresse Oxidativo , Animais , Antioxidantes , Catalase , Glutationa Peroxidase , Masculino , Malondialdeído , Ratos , Ratos Wistar , Superóxido Dismutase , Triazóis/toxicidade
16.
Nan Fang Yi Ke Da Xue Xue Bao ; 40(7): 942-948, 2020 Jul 30.
Artigo em Chinês | MEDLINE | ID: mdl-32895159

RESUMO

OBJECTIVE: To investigate the effect of periostin on hypoxia-induced oxidative stress and apoptosis in human periodontal ligament fibroblasts and the molecular mechanism involved. METHODS: In vitro cultured human periodontal ligament fibroblasts were placed in an anaerobic gas-producing bag for hypoxia treatment for 48 h followed by treatment with periostin at low (25 ng/mL), moderate (50 ng/mL) or high (100 ng/mL) doses. MTT assay was used to measure the cell viability, and the cell apoptosis rate was determined using flow cytometry. The contents of IL-1ß, IL-6 and TNF-α in the cells were determined with ELISA, and ROS levels were measured using a fluorescent plate reader. The intracellular SOD activity was detected using ELISA. The expressions of HIF-1α, P21, cyclin D1, Bax, cleaved caspase-3, Bcl-2, P38MAPK and p-p38 MAPK proteins in the cells were detected with Western blotting. RESULTS: Hypoxia treatment significantly reduced the cell viability (P < 0.05), increased P21, Bax, and cleaved caspase-3 protein levels (P < 0.05), promoted cell apoptosis (P < 0.05), and decreased cyclin D1 and Bcl-2 protein levels (P < 0.05) in the cells. Compared with the hypoxic group, the cells treated with periostin at different concentrations showed significantly increased cell viability (P < 0.05) with significantly lowered apoptotic rates (P < 0.05) and decreased expression levels of Bax and cleaved caspase-3 (P < 0.05) but significantly increased expression levels of cyclin D1 and Bcl-2 (P < 0.05). Hypoxic exposure of the cells resulted in significantly increased expression levels of HIF-1α and p-p38 MAPK (P < 0.05) and increased levels of IL-1ß, IL-6, TNF-α and ROS (P < 0.05) but decreased SOD activity (P < 0.05). Periostin treatment at different concentrations significantly lowered the expression levels of HIF-1α and p-p38 MAPK (P < 0.05) and the levels of IL-1ß, IL-6, TNF-α and ROS (P < 0.05) and significantly increased SOD activity in the hypoxic cells (P < 0.05). CONCLUSIONS: Periostin promotes the proliferation, inhibits apoptosis, enhances cellular antioxidant capacity, and reduces inflammatory damage in human periodontal ligament fibroblasts exposed to hypoxia possibly by inhibiting the activation of the p38 MAPK signaling pathway.


Assuntos
Apoptose , Ligamento Periodontal , Fibroblastos , Humanos , Hipóxia , Estresse Oxidativo , Transdução de Sinais , Proteínas Quinases p38 Ativadas por Mitógeno
17.
Nan Fang Yi Ke Da Xue Xue Bao ; 40(6): 850-855, 2020 Jun 30.
Artigo em Chinês | MEDLINE | ID: mdl-32895208

RESUMO

OBJECTIVE: To investigate the effects of Shoutai pills (a traditional Chinese medicinal preparation) on immune functions and oxidative stress in pregnant rats exposed to di(2-ethylhexyl) phthalate (DEHP). METHODS: Thirty-six mature female SD rats were randomly divided into 3 groups (n=12). After pregnancy was confirmed, the rats were given 10 mL/kg corn oil +10 mL/kg saline (control group), 500 mg/kg DEHP+10 mL/kg saline (model group), and 500 mg/kg DEHP+10 mL/kg Shoutai pills (treatment group). At 19 days of gestation, the rats were sacrificed and the fetal rats were weighed and the numbers of live and stillborn fetal rats were recorded. Serum levels of interleukin-6 (IL-6), interleukin-2 (IL-2), tumor necrosis factor-ɑ (TNF-ɑ), estradiol (E2) and progesterone (P) levels were detected. The appearance, color and quality of the placenta in each group were recorded, and the placental tissues were examined pathologically. The total antioxidant capacity (T-AOC), superoxide dismutase (SOD), glutathione peroxidase (GSH- Px), catalase (CAT), reactive oxygen species (ROS) and malondialdehyde (MDA) in the placental tissues were measured. RESULTS: Compared with the control group, the rats with DEHP exposure showed slow weight gain in the middle and late gestation period and significantly lower fetal weight (P < 0.05) with lowered serum levels of IL-2, IL-6 and TNF-ɑ, increased estradiol level (P < 0.05), decreased placental T-AOC, GSH-Px, SOD and CAT levels, and increased ROS and MDA levels (P < 0.01). Compared with the model group, the rats treated with Shoutai pills had significantly increased weight gain in mid and late pregnancy and greater fetal weight (P < 0.05) with significantly increased serum IL-2 and IL-6 levels, decreased estradiol level (P < 0.05), slightly increased TNF-ɑ expression (P> 0.05), increased placenta T-AOC, GSH- Px and CAT levels, decreased MDA level (P < 0.05), and slightly increased SOD and decreased ROS levels (P>0.05). No significant difference was found in progesterone levels among the groups (P>0.05). HE staining showed that the trophoblast in the placental tissue sponge in the model group was loose and irregular with numerous vacuoles. In the treatment group, the structure of the placenta remained intact with clearly visible labyrinth zone, sponge trophoblast and giant cell trophoblast, and the cell distribution in each layer was better than that in the model group. CONCLUSIONS: Shoutai pills can regulate the immune function of DEHP-exposed pregnant rats possibly by antagonizing the estrogenlike effect of DEHP and regulating serum immune factors; Shoutai pills can also reduce placental tissue damage and improve pregnancy outcome by correcting DEHP-induced imbalance of oxidative stress in the placental tissues.


Assuntos
Estresse Oxidativo , Animais , Dietilexilftalato , Feminino , Ácidos Ftálicos , Gravidez , Ratos , Ratos Sprague-Dawley
18.
Medicine (Baltimore) ; 99(36): e21792, 2020 Sep 04.
Artigo em Inglês | MEDLINE | ID: mdl-32899007

RESUMO

Major lipids making effects on the occurrence of acute ischemic stroke (AIS) is well recognized, but their roles on stroke severity remain uncertain. To explore the exact roles of lipids playing on stroke severity and the possible mechanism, we conduct this observational study.Data was collected from patients with AIS from February 2008 to May 2012. The level of major lipids was compared among AIS groups with different severity and investigated the correlation. Also, the relationship existed between major lipids and bilirubin. Mechanism of major lipids playing on stroke severity was researched to determine if oxidative stress reflected by bilirubin.Lower triglyceride (TG) and higher high density lipoprotein cholesterol (HDL-C) were observed in severe stroke, and obvious correlation existed between TG and stroke severity or HDL-C and stroke severity. TG was associated negatively with direct bilirubin (DBIL) and total bilirubin (TBIL), and lower level of DBIL and TBIL were related to higher quartiles of TG. There was no obvious difference of DBIL and TBIL among the groups of quartiles of HDL-C. TG was the influence factor of stroke severity in severe stroke through multiple univariable logistic regression. But it was not the independent influence factor after multivariable logistic regression adjusted by DBIL or TBIL. However, HDL-C was the influence factor of stroke severity through both univariable and multivariable logistic regression.Lower TG or higher HDL-C predicted severer stroke. The effect of TG on stroke severity was mediated by bilirubin, not HDL-C.


Assuntos
Bilirrubina/sangue , HDL-Colesterol/sangue , Acidente Vascular Cerebral/sangue , Triglicerídeos/sangue , Idoso , Biomarcadores/sangue , Feminino , Humanos , Masculino , Estresse Oxidativo , Índice de Gravidade de Doença
19.
Acta Cir Bras ; 35(8): e202000802, 2020 Sep 04.
Artigo em Inglês | MEDLINE | ID: mdl-32901679

RESUMO

PURPOSE: To investigate the effects of grape seed proanthocyanidin B2 (GSPB2) preconditioning on oxidative stress and apoptosis of renal tubular epithelial cells in mice after renal ischemia-reperfusion (RIR). METHODS: Forty male ICR mice were randomly divided into 4 groups: Group A: mice were treated with right nephrectomy. Group B: right kidney was resected and the left renal vessel was clamped for 45 minutes. Group C: mice were intraperitoneally injected with GSPB2 before RIR established. Group D: mice were intraperitoneally injected with GSPB2 plus brusatol before RIR established. Creatinine and urea nitrogen of mice were determined. Pathological and morphological changes of kidney were checked. Expressions of Nrf-2, HO-1, cleaved-caspase3 were detected by Western-blot. RESULTS: Compared to Group B, morphology and pathological damages of renal tissue were less serious in Group C. Western-blot showed that expressions of Nrf-2 and HO-1 in Group C were obviously higher than those in Group B. The expression of cleaved-caspase3 in Group C was significantly lower than that in Group B. CONCLUSION: GSPB2 preconditioning could attenuate renal oxidative stress injury and renal tubular epithelial cell apoptosis by up-regulating expressions of Nrf-2 and HO-1 and down-regulating the expression of cleaved-caspase-3, but the protective effect could be reversed by brusatol.


Assuntos
Apoptose , Extrato de Sementes de Uva , Estresse Oxidativo , Proantocianidinas , Traumatismo por Reperfusão , Animais , Apoptose/efeitos dos fármacos , Células Epiteliais , Extrato de Sementes de Uva/farmacologia , Extrato de Sementes de Uva/uso terapêutico , Masculino , Camundongos , Camundongos Endogâmicos ICR , Estresse Oxidativo/efeitos dos fármacos , Proantocianidinas/farmacologia , Proantocianidinas/uso terapêutico
20.
Chemosphere ; 258: 127411, 2020 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-32947668

RESUMO

Non-steroidal anti-inflammatory drugs as an important group of emerging environmental contaminants in irrigation water and soils can influence biochemical and physiological processes essential for growth and development in plants as non-target organisms. Plants are able to take up, transport, transform, and accumulate drugs in the roots. Root biomass in ten-days old pea plants was lowered by 6% already under 0.1 mg/L naproxen (NPX) due to a lowered number of lateral roots, although 0.5 mg/L NPX stimulated the total root length by 30% as against control. Higher section area (by 40%) in root tip, area of xylem (by 150%) or stele-to-section ratio (by 10%) in zone of maturation, and lower section area in zone of lateral roots (by 18%) prove the changes in primary root anatomy and its earlier differentiation at 10 mg/L NPX. Accumulated NPX (up to 10 µg/g DW at 10 mg/L) and products of its metabolization in roots increased the amounts of hydrogen peroxide (by 33%), and superoxide (by 62%), which was reflected in elevated lipid peroxidation (by 32%), disruption of membrane integrity (by 89%) and lowering both oxidoreductase and dehydrogenase activities (by up to 40%). Elevated antioxidant capacity (SOD, APX, and other molecules) under low treatments decreased at 10 mg/L NPX (both by approx. 30%). Naproxen was proved to cause changes at both cellular and tissue levels in roots, which was also reflected in their anatomy and morphology. Higher environmental loading through drugs thus can influence even the root function.


Assuntos
Anti-Inflamatórios não Esteroides/toxicidade , Naproxeno/toxicidade , Ervilhas/fisiologia , Antioxidantes/metabolismo , Peróxido de Hidrogênio/metabolismo , Peroxidação de Lipídeos , Estresse Oxidativo/efeitos dos fármacos , Ervilhas/efeitos dos fármacos , Raízes de Plantas
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