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[PMID]:29175398
[Au] Autor:Qiu N; Wang R; Sun Y; Wang X; Jiang D; Meng Y; Zhou F
[Ad] Endereço:School of Life Science, Qufu Normal University, Qufu, Shandong 273165, China.
[Ti] Título:Toxic effects and mechanism of 2,2',4,4'-tetrabromodiphenyl ether (BDE-47) on Lemna minor.
[So] Source:Chemosphere;193:711-719, 2018 Feb.
[Is] ISSN:1879-1298
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:To investigate the toxic effect and mechanism of 2,2',4,4'-tetrabromodiphenyl ether (BDE-47) in aquatic plants, in vivo and in vitro exposure to BDE-47 were conducted. After 14-d exposure to 5-20 µg/L BDE-47, the growth of Lemna minor plants was significantly suppressed, and the chlorophyll and soluble protein contents in fronds markedly decreased. Accordingly, the photosynthetic efficiency (Fv/Fm, PI) decreased. When the thylakoid membranes isolated from healthy fronds was exposed to 5-20 mg/L BDE-47 directly in vitro for 1 h, the photosynthetic efficiency also decreased significantly. In both the in vitro (5-20 µg/L) and in vivo (5-20 mg/L) experiments, BDE-47 led to an increased plasma membrane permeability. Hence, we concluded that BDE-47 had a direct toxicity to photosynthetic membranes and plasma membranes. However, direct effects on the activities of peroxidase (POD), malate dehydrogenase (MDH) and nitroreductase (NR) were not observed by adding 5-20 mg/L BDE-47 into crude enzyme extracts. The malondialdehyde (MDA) and superoxide anion radical (O ) contents in the BDE-47 treated fronds were higher than those in the control fronds, suggesting that L. minor can not effectively relieve reactive oxygen species (ROS). The data above indicates that BDE-47 is toxic to L. minor through acting directly on biomembranes, which induces the production of ROS and thus causes remarkable oxidative damage to cells.
[Mh] Termos MeSH primário: Araceae/efeitos dos fármacos
Éteres Difenil Halogenados/toxicidade
Poluentes Químicos da Água/toxicidade
[Mh] Termos MeSH secundário: Araceae/enzimologia
Araceae/metabolismo
Clorofila/metabolismo
Éter
Malondialdeído/metabolismo
Oxirredução
Peroxidase/metabolismo
Espécies Reativas de Oxigênio/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Halogenated Diphenyl Ethers); 0 (Reactive Oxygen Species); 0 (Water Pollutants, Chemical); 0F5N573A2Y (Ether); 0N97R5X10X (2,2',4,4'-tetrabromodiphenyl ether); 1406-65-1 (Chlorophyll); 4Y8F71G49Q (Malondialdehyde); EC 1.11.1.7 (Peroxidase)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171128
[St] Status:MEDLINE


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[PMID]:29441915
[Au] Autor:Cao L-; Yan M; Ma YX; Zhang BK; Fang PF; Xiang DX; Li ZH; Gong H; Deng Y; Li HD
[Ti] Título:Isoliquiritigenin protects against triptolide-induced hepatotoxicity in mice through Nrf2 activation.
[So] Source:Pharmazie;71(7):394-397, 2016 Jul 07.
[Is] ISSN:0031-7144
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Isoliquiritigenin, a flavonoid found in licorice, has been considered as an antioxidive and hepato-protective agent. Recent studies have shown that a possible mechanism for triptolide-induced hepatotoxicity is related to oxidative damage induced by reactive oxygen species. This study was done to investigate the protection effect of isoliquiritigenin against triptolide-induced hepatotoxicity and the mechanism involved. An acute liver injury model was established by intraperitoneal injection of triptolide (1.0 mg · kg-1) in mice. Different doses of isoliquiritigenin (12.5, 25 and 50 mg · kg-1) were employed as protection. The activities of AST, ALT, ALP and LDH in serum and levels of GSH, GPx, SOD, CAT and MDA in liver tissue were detected. The histopathological changes of liver tissues were observed after HE staining. The protein expression of Nrf2 was detected by western blot. Pretreatment with isoliquiritigenin significantly prevented the triptolide-induced hepatotoxicity indicated by reduced activities of AST, ALT, ALP and LDH. Moreover, isoliquiritigenin pretreatment also prevented from triptolide-induced hepatotoxicity by inhibiting MDA and restoring the levels of GSH, GPx, SOD and CAT. In addition, isoliquiritigenin could attenuate histopathological changes induced by triptolide. Furthermore, the results indicated that isoliquiritigenin pretreatment caused an increase in the protein expression of Nrf2. These results indicated that isoliquiritigenin could protect against triptolide-induced hepatotoxicity via activation of the Nrf2 pathway.
[Mh] Termos MeSH primário: Chalconas/farmacologia
Doença Hepática Induzida por Substâncias e Drogas/prevenção & controle
Diterpenos/antagonistas & inibidores
Diterpenos/toxicidade
Fator 2 Relacionado a NF-E2/metabolismo
Fenantrenos/antagonistas & inibidores
Fenantrenos/toxicidade
Substâncias Protetoras/farmacologia
[Mh] Termos MeSH secundário: Animais
Doença Hepática Induzida por Substâncias e Drogas/patologia
Compostos de Epóxi/antagonistas & inibidores
Compostos de Epóxi/toxicidade
Fígado/efeitos dos fármacos
Fígado/metabolismo
Testes de Função Hepática
Masculino
Malondialdeído/antagonistas & inibidores
Camundongos
Camundongos Endogâmicos ICR
Fator 2 Relacionado a NF-E2/efeitos dos fármacos
Estresse Oxidativo/efeitos dos fármacos
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Chalcones); 0 (Diterpenes); 0 (Epoxy Compounds); 0 (NF-E2-Related Factor 2); 0 (Nfe2l2 protein, mouse); 0 (Phenanthrenes); 0 (Protective Agents); 19ALD1S53J (triptolide); 4Y8F71G49Q (Malondialdehyde); B9CTI9GB8F (isoliquiritigenin)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180215
[St] Status:MEDLINE
[do] DOI:10.1691/ph.2016.6535


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[PMID]:29267671
[Au] Autor:Lutfioglu M; Aydogdu A; Atabay VE; Sakallioglu EE; Avci B
[Ad] Endereço:Ondokuz Mayis University Faculty of Dentistry, Department of Periodontology, Samsun, Turkey.
[Ti] Título:Gingival crevicular fluid oxidative stress level in patients with periodontal disease and hyperlipidemia.
[So] Source:Braz Oral Res;31:e110, 2017 Dec 18.
[Is] ISSN:1807-3107
[Cp] País de publicação:Brazil
[La] Idioma:eng
[Ab] Resumo:This study aimed to assess the impact of hyperlipidemia on healthy and diseased periodontal tissue by evaluating oxidative stress biomarkers in gingival crevicular fluid (GCF). Clinical periodontal parameters and blood serum lipid, GCF malondialdehyde (MDA), protein carbonyl (PC), and total antioxidant capacity (TAOC) levels were evaluated in six age and sex-matched groups (n = 15 each) of normolipidemic and hyperlipidemic individuals as follows: normolipidemic + periodontally healthy (H), normolipidemic + gingivitis (G), normolipidemic + chronic periodontitis (CP), hyperlipidemic + periodontally healthy (HH), hyperlipidemic + gingivitis (HG), and hyperlipidemic + CP (HCP). GCF MDA, and PC levels varied among groups, with patients with periodontitis having the highest MDA and PC levels [CP > G > H (p < 0.01) and HCP > HG > HH (p < 0.01)] and the lowest TAOC levels [CP < G < H (p < 0.01) and HCP < HG < HH (p < 0.01)]. Furthermore, paired comparisons showed MDA and PC levels to be higher and TAOC levels to be lower in HCP compared with NCP (p < 0.01). In patients with hyperlipidemia, GCF, MDA, and PC levels positively correlated with clinical assessments and serum triglycerides (TG), total cholesterol (TC), and low-density lipoprotein cholesterol (LDL) levels and negatively correlated with serum high-density lipoprotein cholesterol (HDL) levels, whereas GCF TAOC levels negatively correlated with clinical assessments and serum TG, TC, and LDL levels, but positively correlated with serum HDL levels (p < 0.01). In normolipidemic patients, GCF, MDA, and PC levels positively correlated with clinical assessments and serum TG levels and negatively correlated with serum HDL levels, whereas GCF TAOC levels negatively correlated with clinical assessments and serum TG levels and positively correlated with serum HDL levels (p < 0.01). In conclusion, abnormal serum lipid subfractions could be considered a risk factor for enhancing oxidative stress in GCF in the presence of periodontal disease.
[Mh] Termos MeSH primário: Periodontite Crônica/sangue
Líquido do Sulco Gengival/metabolismo
Gengivite/sangue
Hiperlipidemias/sangue
Estresse Oxidativo/fisiologia
[Mh] Termos MeSH secundário: Adulto
Análise de Variância
Estudos de Casos e Controles
Colesterol/sangue
Periodontite Crônica/etiologia
Ensaio de Imunoadsorção Enzimática
Feminino
Gengivite/etiologia
Seres Humanos
Hiperlipidemias/complicações
Masculino
Malondialdeído/sangue
Meia-Idade
Carbonilação Proteica/fisiologia
Valores de Referência
Estatísticas não Paramétricas
Triglicerídeos/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Triglycerides); 4Y8F71G49Q (Malondialdehyde); 97C5T2UQ7J (Cholesterol)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:D; IM
[Da] Data de entrada para processamento:171222
[St] Status:MEDLINE


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[PMID]:29248874
[Au] Autor:Ma J; Li Y; Wu M; Li X
[Ad] Endereço:College of Life Science, Henan Normal University, Xinxiang, Henan 453007, China.
[Ti] Título:Oxidative stress-mediated p53/p21 pathway may be involved in microcystin-LR-induced cytotoxicity in HepG2 cells.
[So] Source:Chemosphere;194:773-783, 2018 Mar.
[Is] ISSN:1879-1298
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:A previous study showed that microcystin-LR (MC-LR) exerted cytotoxicity and induced apoptosis in HepG2 cells. In the present study, we investigated whether oxidative stress-mediated p53/p21 is involved in this process to further elucidate the mechanism of cytotoxicity induced by MC-LR. Morphological evaluation showed that MC-LR induced time- and dose-dependent cytotoxicity in HepG2 cells. Biochemical assays revealed that MC-LR exposure altered the protein levels of HSP70 and HSP90, generally inhibited superoxide dismutase and catalase, reduced glutathione content, and increased the cellular malondialdehyde level of HepG2 cells, suggesting that MC-LR may induce biochemical disturbance and oxidative stress in HepG2 cells. The protein levels of p-p53 and p21 were markedly increased by MC-LR exposure in a concentration-dependent manner, suggesting that p53 and p21 may be involved in the process. Moreover, we also found that the proto-oncogene c-myc was significantly activated in HepG2 cells following MC-LR exposure, indicating that c-myc in HepG2 cells was potentially involved in response to MC-LR-induced apoptosis. These findings may contribute to further understanding the in vitro molecular mechanism of MC-LR hepatotoxicity.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Inibidor de Quinase Dependente de Ciclina p21/metabolismo
Microcistinas/farmacologia
Estresse Oxidativo/efeitos dos fármacos
Proteína Supressora de Tumor p53/metabolismo
[Mh] Termos MeSH secundário: Catalase/metabolismo
Glutationa/metabolismo
Células Hep G2
Seres Humanos
Malondialdeído/metabolismo
Proteínas Proto-Oncogênicas c-myc/metabolismo
Superóxido Dismutase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CDKN1A protein, human); 0 (Cyclin-Dependent Kinase Inhibitor p21); 0 (MYC protein, human); 0 (Microcystins); 0 (Proto-Oncogene Proteins c-myc); 0 (Tumor Suppressor Protein p53); 4Y8F71G49Q (Malondialdehyde); EC 1.11.1.6 (Catalase); EC 1.15.1.1 (Superoxide Dismutase); EQ8332842Y (cyanoginosin LR); GAN16C9B8O (Glutathione)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180228
[Lr] Data última revisão:
180228
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171218
[St] Status:MEDLINE


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[PMID]:29329335
[Au] Autor:Kyrklund M; Kummu O; Kankaanpää J; Akhi R; Nissinen A; Turunen SP; Pussinen P; Wang C; Hörkkö S
[Ad] Endereço:Medical Microbiology and Immunology, Research Unit of Biomedicine, Faculty of Medicine, University of Oulu, Oulu, Finland.
[Ti] Título:Immunization with gingipain A hemagglutinin domain of Porphyromonas gingivalis induces IgM antibodies binding to malondialdehyde-acetaldehyde modified low-density lipoprotein.
[So] Source:PLoS One;13(1):e0191216, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Treatment of periodontitis has beneficial effects on systemic inflammation markers that relate to progression of atherosclerosis. We aimed to investigate whether immunization with A hemagglutinin domain (Rgp44) of Porphyromonas gingivalis (Pg), a major etiologic agent of periodontitis, would lead to an antibody response cross-reacting with oxidized low-density lipoprotein (OxLDL) and how it would affect the progression of atherosclerosis in low-density lipoprotein receptor-deficient (LDLR-/-) mice. The data revealed a prominent IgM but not IgG response to malondialdehyde-acetaldehyde modified LDL (MAA-LDL) after Rgp44 and Pg immunizations, implying that Rgp44/Pg and MAA adducts may share cross-reactive epitopes that prompt IgM antibody production and consequently confer atheroprotection. A significant negative association was observed between atherosclerotic lesion and plasma IgA to Rgp44 in Rgp44 immunized mice, supporting further the anti-atherogenic effect of Rgp44 immunization. Plasma IgA levels to Rgp44 and to Pg in both Rgp44- and Pg-immunized mice were significantly higher than those in saline control, suggesting that IgA to Rgp44 could be a surrogate marker of immunization in Pg-immunized mice. Distinct antibody responses in plasma IgA levels to MAA-LDL, to Pg lipopolysaccharides (Pg-LPS), and to phosphocholine (PCho) were observed after Rgp44 and Pg immunizations, indicating that different immunogenic components between Rpg44 and Pg may behave differently in regard of their roles in the development of atherosclerosis. Immunization with Rgp44 also displayed atheroprotective features in modulation of plaque size through association with plasma levels of IL-1α whereas whole Pg bacteria achieved through regulation of anti-inflammatory cytokine levels of IL-5 and IL-10. The present study may contribute to refining therapeutic approaches aiming to modulate immune responses and inflammatory/anti-inflammatory processes in atherosclerosis.
[Mh] Termos MeSH primário: Adesinas Bacterianas/imunologia
Anticorpos Antibacterianos/biossíntese
Proteínas de Bactérias/imunologia
Cisteína Endopeptidases/imunologia
Imunoglobulina M/biossíntese
Lipoproteínas LDL/imunologia
Porphyromonas gingivalis/imunologia
[Mh] Termos MeSH secundário: Acetaldeído/análogos & derivados
Adesinas Bacterianas/química
Animais
Anticorpos Antibacterianos/metabolismo
Aterosclerose/etiologia
Aterosclerose/imunologia
Aterosclerose/prevenção & controle
Proteínas de Bactérias/química
Infecções por Bacteroidaceae/complicações
Infecções por Bacteroidaceae/imunologia
Infecções por Bacteroidaceae/microbiologia
Reações Cruzadas
Cisteína Endopeptidases/química
Modelos Animais de Doenças
Feminino
Seres Humanos
Imunização
Imunoglobulina M/metabolismo
Lectinas/química
Lectinas/imunologia
Lipoproteínas LDL/química
Malondialdeído/análogos & derivados
Malondialdeído/imunologia
Camundongos
Camundongos Knockout
Periodontite/complicações
Periodontite/imunologia
Periodontite/microbiologia
Domínios Proteicos
Receptores de LDL/deficiência
Receptores de LDL/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Adhesins, Bacterial); 0 (Antibodies, Bacterial); 0 (Bacterial Proteins); 0 (Immunoglobulin M); 0 (Lectins); 0 (Lipoproteins, LDL); 0 (Receptors, LDL); 0 (hemagglutinin A, Porphyromonas gingivalis); 0 (malondialdehyde-low density lipoprotein, mouse); 4Y8F71G49Q (Malondialdehyde); EC 3.4.22.- (Cysteine Endopeptidases); EC 3.4.22.37 (argingipain, Porphyromonas gingivalis); GO1N1ZPR3B (Acetaldehyde)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180113
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191216


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[PMID]:28469096
[Au] Autor:Wang XN; Zhang CJ; Diao HL; Zhang Y
[Ad] Endereço:Reproductive Medical Center of Renmin Hospital, Hubei University of Medicine, Shiyan, Hubei 442000, China.
[Ti] Título:Protective Effects of Curcumin against Sodium Arsenite-induced Ovarian Oxidative Injury in a Mouse Model.
[So] Source:Chin Med J (Engl);130(9):1026-1032, 2017 May 05.
[Is] ISSN:0366-6999
[Cp] País de publicação:China
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Excessive reactive oxygen species (ROS) may lead to a number of reproductive diseases such as polycystic ovary syndrome. This study aimed to establish an animal model of ovarian oxidative stress and to assess the protective effect of curcumin against oxidative injury. METHODS: Ovarian oxidative stress was induced in female Kunming mice (n = 40) with intraperitoneal injection of 8 mg/kg sodium arsenite (As) once every other day for 16 days; meanwhile, they were, respectively, treated by intragastric administration of 0, 100, 150, or 200 mg/kg (n = 10/group) curcumin once per day for 21 days. Ten normal mice were used as control. Then, the mice were injected intraperitoneally with BrdU and sacrificed; the right ovaries were collected for hematoxylin and eosin (HE) staining and BrdU immunohistochemistry, and the left ovaries for enzyme-linked immunosorbent assay (ELISA) and Western blotting analyses. RESULTS: The ELISA results showed that ROS (11.74 ± 0.65 IU/mg in 8 mg/kg AS + 0 mg/kg curcumin group vs. 10.71 ± 0.91 IU/mg in control group, P= 0.021) and malondialdehyde (MDA) (0.32 ± 0.02 nmol/g in 8 mg/kg AS + 0 mg/kg curcumin group vs. 0.27 ± 0.02 nmol/g in control group, P= 0.048) increased while superoxide dismutase (SOD) (3.96 ± 0.36 U/mg in 8 mg/kg AS + 0 mg/kg curcumin group vs. 4.51 ± 0.70 U/mg in control group, P= 0.012) and glutathione peroxidase (17.36 ± 1.63 U/g in 8 mg/kg AS + 0 mg/kg curcumin group vs. 18.92 ± 1.80 U/g in control group, P= 0.045) decreased in the ovary after injection of As, indicating successful modeling of oxidative stress. Curcumin treatment could considerably increase SOD (4.57 ± 0.68, 4.49 ± 0.27, and 4.56 ± 0.25 U/mg in 100 mg/kg, 150 mg/kg, and 200 mg/kg curcumin group, respectively, allP < 0.05) while significantly reduce ROS (10.64 ± 1.38, 10.73 ± 0.71, and 10.67 ± 1.38 IU/mg in 100 mg/kg, 150 mg/kg, and 200 mg/kg curcumin group, respectively, allP < 0.05) and MDA (0.28 ± 0.02, 0.25 ± 0.03, and 0.27 ± 0.04 nmol/g in 100 mg/kg, 150 mg/kg, and 200 mg/kg curcumin group, respectively; bothP < 0.05) in the ovary. HE staining and BrdU immunohistochemistry of the ovarian tissues indicated the increased amount of atretic follicles (5.67 ± 0.81, 5.84 ± 0.98, and 5.72 ± 0.84 in 100 mg/kg, 150 mg/kg, and 200 mg/kg curcumin group, respectively, all P < 0.05), and the inhibited proliferation of granular cells under oxidative stress would be reversed by curcumin. Furthermore, the Western blotting of ovarian tissues showed that the p66Shc expression upregulated under oxidative stress would be lowered by curcumin. CONCLUSION: Curcumin could alleviate arsenic-induced ovarian oxidative injury to a certain extent.
[Mh] Termos MeSH primário: Arsenitos/toxicidade
Curcumina/uso terapêutico
Compostos de Sódio/toxicidade
[Mh] Termos MeSH secundário: Animais
Modelos Animais de Doenças
Ensaio de Imunoadsorção Enzimática
Feminino
Glutationa Peroxidase/metabolismo
Imuno-Histoquímica
Malondialdeído/metabolismo
Camundongos
Ovário/efeitos dos fármacos
Ovário/metabolismo
Estresse Oxidativo/efeitos dos fármacos
Síndrome do Ovário Policístico/tratamento farmacológico
Síndrome do Ovário Policístico/metabolismo
Espécies Reativas de Oxigênio/metabolismo
Superóxido Dismutase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Arsenites); 0 (Reactive Oxygen Species); 0 (Sodium Compounds); 48OVY2OC72 (sodium arsenite); 4Y8F71G49Q (Malondialdehyde); EC 1.11.1.9 (Glutathione Peroxidase); EC 1.15.1.1 (Superoxide Dismutase); IT942ZTH98 (Curcumin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.4103/0366-6999.204927


  7 / 22085 MEDLINE  
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[PMID]:28455127
[Au] Autor:Camini FC; da Silva Caetano CC; Almeida LT; da Costa Guerra JF; de Mello Silva B; de Queiroz Silva S; de Magalhães JC; de Brito Magalhães CL
[Ad] Endereço:Núcleo de Pesquisas em Ciências Biológicas, NUPEB, Universidade Federal de Ouro Preto, Ouro Preto, Minas Gerais, Brazil.
[Ti] Título:Oxidative stress in Mayaro virus infection.
[So] Source:Virus Res;236:1-8, 2017 05 15.
[Is] ISSN:1872-7492
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Mayaro virus (MAYV) is a neglected tropical arbovirus that causes a febrile syndrome that is sometimes accompanied by incapacitating arthritis/arthralgia. The pathogenesis of MAYV has not been completely defined and oxidative stress mediated by an increase in reactive oxygen species (ROS) and/or depletion of antioxidant defences has been found to contribute to several aspects of viral disease. To investigate whether MAYV induced oxidative stress in host cells, we monitored ROS production, oxidative stress markers and antioxidant defences at different time points after infection. Our results show that MAYV induced significant oxidative stress in infected HepG2 cells, as indicated by the increase of malondialdehyde (MDA) and protein carbonyl levels, and by a significant decrease of the reduced versus oxidized glutathione (GSH/GSSG) ratio. Generally, MAYV-infected HepG2 cells also showed an increase in antioxidant defences. We observed an increase in the superoxide dismutase (SOD) and catalase (CAT) activities and the total glutathione content. To determine whether similar effects occurred in other cell types, we evaluated the ROS, MDA and SOD activity levels in J774 cells after MAYV infection. Similar to our observations in HepG2 cells, the J774 cells showed an increase in ROS, MDA and total SOD activity following MAYV infection. Thus, since the cellular redox environment is influenced by the production and removal of ROS, we hypothesize that the overproduction of ROS was responsible for the oxidative stress in response to the MAYV infection despite the increase in the antioxidant status. This study is the first report on the involvement of oxidative stress during MAYV infection. Collectively, our data shed light on some mechanisms that are operational in host cells following exposure to MAYV.
[Mh] Termos MeSH primário: Infecções por Alphavirus/metabolismo
Alphavirus/fisiologia
Estresse Oxidativo
[Mh] Termos MeSH secundário: Alphavirus/genética
Infecções por Alphavirus/genética
Infecções por Alphavirus/virologia
Catalase/metabolismo
Glutationa/metabolismo
Células Hep G2
Seres Humanos
Malondialdeído/metabolismo
Oxirredução
Espécies Reativas de Oxigênio/metabolismo
Superóxido Dismutase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Reactive Oxygen Species); 4Y8F71G49Q (Malondialdehyde); EC 1.11.1.6 (Catalase); EC 1.15.1.1 (Superoxide Dismutase); GAN16C9B8O (Glutathione)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170430
[St] Status:MEDLINE


  8 / 22085 MEDLINE  
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[PMID]:29353699
[Au] Autor:Abdel-Magied N; Ahmed AG; Shedid SM
[Ad] Endereço:Radiation Biology Research, National Centre for Radiation Research and Technology (NCRRT), Atomic Energy Authority, 3st Ahmed Elzomer, Nasr city, Cairo, Egypt. Electronic address: nanyabdelmagid@yahoo.com.
[Ti] Título:Near-infrared heat lamp therapeutic effect on paraoxonase 1 and myeloperoxidase as potential biomarkers of redox state changes induced by γ-irradiation in albino rats.
[So] Source:J Photochem Photobiol B;179:105-112, 2018 Feb.
[Is] ISSN:1873-2682
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Infrared radiation has a potential therapeutic effect in some diseases. The aim of this study was to estimate the therapeutic role of near infrared heat lamp (NIRHL) on the variations of the activity of paraoxonase 1 (PON1) and myeloperoxidase (MPO), in relation to lipid disorders, associated with oxidative stress in rats gamma-irradiated. In addition, study the effect of the duration of NIRHL treatment. Animals were divided into six groups. The results revealed that irradiated rats treated with NIRHL 20 min/once/day showed positive modulation of PON1 and MPO linked to significant improvement of lipid disorders evidenced by lower triglycerides, low density lipoprotein cholesterol (LDL-C), oxidized low density lipoprotein cholesterol (oxLDL-C) and higher density lipoprotein cholesterol (HDL-C) as well as significant amelioration of redox state, manifested by markedly increase of glutathione (GSH) content, total antioxidant capacity (TAC) associated with a noticeable decrease of pro-inflammatory cytokines. (TNF-α, IL-1 beta and IL-6), nitric oxide (NO), nitric oxide synthase (NOs), malondialdehyde (MDA), compared to irradiated rats. The results showed also that the NIRHL treatment for 20 min/twice/day had negative effects on the previous parameters and on the behavior of rats such as itching, irritability, dyspnea and death in normal as well as, irradiated rats. In conclusion, the results in this study show that NIRHL therapy for a short time can effectively prevent the lipid disorders induced by radiation through the positive modulation mechanism of PON1 and MPO enzymes and improvement of oxidative stress.
[Mh] Termos MeSH primário: Arildialquilfosfatase/metabolismo
Biomarcadores/metabolismo
Raios Infravermelhos
Peroxidase/metabolismo
[Mh] Termos MeSH secundário: Animais
Cálcio/análise
HDL-Colesterol/sangue
LDL-Colesterol/sangue
Citocinas/metabolismo
Raios gama
Glutationa/sangue
Masculino
Malondialdeído/sangue
Óxido Nítrico/sangue
Oxirredução
Ratos
Ratos Sprague-Dawley
Temperatura Ambiente
Irradiação Corporal Total
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Cholesterol, HDL); 0 (Cholesterol, LDL); 0 (Cytokines); 31C4KY9ESH (Nitric Oxide); 4Y8F71G49Q (Malondialdehyde); EC 1.11.1.7 (Peroxidase); EC 3.1.8.1 (Aryldialkylphosphatase); GAN16C9B8O (Glutathione); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180223
[Lr] Data última revisão:
180223
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180123
[St] Status:MEDLINE


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[PMID]:29254287
[Au] Autor:Jiang L; Li H; Zhao N
[Ad] Endereço:Department of Anesthesiology, No. 215 Hospital of Shaanxi Nuclear Industry, Xianyang, Shaanxi, China.
[Ti] Título:Thymoquinone protects against cobalt chloride-induced neurotoxicity via Nrf2/GCL-regulated glutathione homeostasis.
[So] Source:J Biol Regul Homeost Agents;31(4):843-853, 2017 Oct-Dec.
[Is] ISSN:0393-974X
[Cp] País de publicação:Italy
[La] Idioma:eng
[Ab] Resumo:The prevalence of neurodegenerative diseases worldwide has increased dramatically in the last decades. Hypoxia and oxidative stress play a central role in the pathogenesis of neurodegenerative diseases. Thymoquinone (TQ) is a monoterpenoid hydrocarbon compound that possesses potent antioxidant activity. In the current study, we investigated the neuroprotective effects of TQ against CoCl2, a widely used hypoxia-inducing agent. We found that TQ inhibited CoCl2-indcued cytotoxicity in vitro, as reflected by an increase of cell viability and decrease of apoptosis in CoCl2-treated PC12 cells. TQ exhibited a potent protective effect against CoCl2-induced neurotoxicity in vivo, as evidenced by decreased time spent to find the platform site in the Probe trials, reduced escape latencies, decreased traveling distance and reduction of apoptotic cell death in brains in CoCl2-treated rats. CoCl2-resulted decrease of glutathione (GSH) and increase of malondialdehyde (MDA) levels were significantly inhibited by TQ. Inhibition of GSH synthesis by buthionine sulphoximine (BSO) significantly attenuated TQ-induced neuroprotective effects against CoCl2 in rats and in PC12 cells. TQ could upregulate nuclear factor (erythroid-derived 2)-like 2 (Nrf2)/glutamate-cysteine ligase catalytic subunit (GCLc) and Nrf2/glutamate-cysteine ligase modifier subunit (GCLm) pathway which contributed to antioxidant and neuroprotective effects of TQ. In summary, we found that TQ exhibited protective effects against neurotoxicity via upregulation of Nrf2/GCL signaling. Upregulation of Nrf2/GCL signaling promoted the synthesis of GSH and contributed to attenuation of oxidative stress, neuronal cell apoptosis and neurotoxicity. These data have appointed a new path toward the understanding of the neuroprotective activities of TQ.
[Mh] Termos MeSH primário: Antioxidantes/farmacologia
Benzoquinonas/farmacologia
Cobalto/farmacologia
Hipóxia/prevenção & controle
Fármacos Neuroprotetores/farmacologia
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Butionina Sulfoximina/antagonistas & inibidores
Butionina Sulfoximina/farmacologia
Hipóxia Celular/efeitos dos fármacos
Sobrevivência Celular/efeitos dos fármacos
Comportamento Exploratório/efeitos dos fármacos
Regulação da Expressão Gênica/efeitos dos fármacos
Glutamato-Cisteína Ligase/genética
Glutamato-Cisteína Ligase/metabolismo
Glutationa/agonistas
Glutationa/metabolismo
Seres Humanos
Hipóxia/induzido quimicamente
Hipóxia/genética
Hipóxia/patologia
Masculino
Malondialdeído/antagonistas & inibidores
Malondialdeído/metabolismo
Fator 2 Relacionado a NF-E2/genética
Fator 2 Relacionado a NF-E2/metabolismo
Células PC12
Ratos
Ratos Wistar
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antioxidants); 0 (Benzoquinones); 0 (NF-E2-Related Factor 2); 0 (Neuroprotective Agents); 0 (Nfe2l2 protein, rat); 3G0H8C9362 (Cobalt); 490-91-5 (thymoquinone); 4Y8F71G49Q (Malondialdehyde); 5072-26-4 (Buthionine Sulfoximine); EC 6.3.2.2 (GCLM protein, rat); EC 6.3.2.2 (Glutamate-Cysteine Ligase); EC 6.3.2.2. (GCLC protein, rat); EVS87XF13W (cobaltous chloride); GAN16C9B8O (Glutathione)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171220
[St] Status:MEDLINE


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[PMID]:29381287
[Au] Autor:Bakirov AB; Badamshina GG; Timasheva GV; Karimova LK; Valeeva ET; Galimova RR; Daukaev RA; Grigoryeva LM
[Ti] Título:[The use of the antioxidant drink by healthy workers exposed to chemical factors].
[So] Source:Vopr Pitan;85(4):82-6, 2016.
[Is] ISSN:0042-8833
[Cp] País de publicação:Russia (Federation)
[La] Idioma:rus
[Ab] Resumo:In chemical manufacturing along with alimentary factors, workers are exposed to occupational hazards resulting in reduced antitoxic protective properties of the organism. The purpose of the present work was to develop a preventive method for reducing antitoxic functions of the body of healthy workers exposed to chemical factors. We have produced the drink containing carrot juice, honey, olive oil. The study involved 50 employees (the average age was 37.4±5.5 years) with experience of over 15 years. The main group (25 people) were workers with reduced antitoxic function who received the drink before each day's work shift for 10 days, the control group - workers with normal anti-toxic function, which did not take a drink. It was found that antioxidant drink intake by healthy employees of a chemical complex lead to the decrease of the level of molecules of average mass at λ=254 nm and at λ=280 nm by 15.1±7.2%, the activity of gammaglutamyl transferase - by 19.1%, alaninaminotransferase - by 44.1%, aspartataminotrans-ferase - by 34.7% (indicators of the syndrome of endogenous intoxication), the decrease of the content of malondialdehyde (as an indicator of an excessive accumulation of products of lipid peroxidation) - by 43.8%, while the activity of catalase, that indicates an increase in the antitoxic functions of the organism, increased by 37.5%.
[Mh] Termos MeSH primário: Antioxidantes/administração & dosagem
Bebidas
Indústria Química
Malondialdeído/sangue
Exposição Ocupacional/efeitos adversos
Oxirredutases/sangue
[Mh] Termos MeSH secundário: Adulto
Feminino
Seres Humanos
Masculino
[Pt] Tipo de publicação:CLINICAL TRIAL; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antioxidants); 4Y8F71G49Q (Malondialdehyde); EC 1.- (Oxidoreductases)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180216
[Lr] Data última revisão:
180216
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180131
[St] Status:MEDLINE



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