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[PMID]:29175396
[Au] Autor:Wang F; Liu F; Chen W; Xu R; Wang W
[Ad] Endereço:School of Biological Science, Luoyang Normal University, Luoyang, 471022, China; Cold Water Fish Breeding Engineering Technology Research Center of Henan Province, Luoyang, 471022, China. Electronic address: wangfan7677@163.com.
[Ti] Título:Effects of triclosan (TCS) on hormonal balance and genes of hypothalamus-pituitary- gonad axis of juvenile male Yellow River carp (Cyprinus carpio).
[So] Source:Chemosphere;193:695-701, 2018 Feb.
[Is] ISSN:1879-1298
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Triclosan (TCS) is a broad spectrum antimicrobial agent which has been widely dispersed and determinated in the aquatic environment. However, the effects of TCS on reproductive endocrine in male fish are poorly understood. In this study, male Yellow River carp (Cyprinus carpio) were exposed to 0, 1/5, 1/10 and 1/20 LC (96 h LC of TCS to carp) TCS under semi-static conditions for 42 d. Vitellogenin (Vtg), 17ß-estradiol (E ), testosterone(T), gonadotropin (GtH), and gonadotropin-releasing hormone (GnRH) levels were measured by enzyme-linked immunosorbent assay (ELISA). Meanwhile, we also examined the mRNA expressions of aromatase, GtHs-ß, GnRH, estrogen receptor (Er), and androgen receptor (Ar) by quantitative Real-time Polymerase Chain Reaction (qRT-PCR). TCS induced Vtg levels of hepatopancreas, E levels of serum, and inhibited Ar and Er mRNA levels, suggesting that the induction of Vtg production by TCS was indirectly caused by non-Er pathways. TCS-induced Vtg levels by interfering with the reproductive axis at plenty of latent loci of male carps: (a) TCS exposure increased the aromatase mRNA expression of hypothalamus and gonad aromatase, consequently increasing serum concentrations of E to induce Vtg in hepatopancreas; (b) TCS treatment changed GtH-ß and GnRH mRNA expression and secretion, causing the disturbance of reproductive endocrine; (c) TCS exposure decreased Ar mRNA levels, indicating potential Ar-mediated antiandrogen action. These mechanisms showed that TCS may induce Vtg production in male carp by non-Er-mediated pathways.
[Mh] Termos MeSH primário: Carpas/metabolismo
Triclosan/toxicidade
Poluentes Químicos da Água/toxicidade
[Mh] Termos MeSH secundário: Animais
Anti-Infecciosos/toxicidade
Aromatase/genética
Sistema Endócrino/efeitos dos fármacos
Ensaio de Imunoadsorção Enzimática
Estradiol/análise
Hormônio Liberador de Gonadotropina/análise
Hormônio Liberador de Gonadotropina/genética
Gônadas/enzimologia
Gônadas/metabolismo
Hepatopâncreas/metabolismo
Hormônios/metabolismo
Hipotálamo/metabolismo
Masculino
Hipófise/metabolismo
RNA Mensageiro/análise
Reação em Cadeia da Polimerase em Tempo Real
Receptores Estrogênicos/genética
Reprodução/efeitos dos fármacos
Testosterona/análise
Vitelogeninas/análise
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Infective Agents); 0 (Hormones); 0 (RNA, Messenger); 0 (Receptors, Estrogen); 0 (Vitellogenins); 0 (Water Pollutants, Chemical); 33515-09-2 (Gonadotropin-Releasing Hormone); 3XMK78S47O (Testosterone); 4NM5039Y5X (Triclosan); 4TI98Z838E (Estradiol); EC 1.14.14.1 (Aromatase); EC 1.14.14.1 (CYP19A1 protein, human)
[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]:29339527
[Au] Autor:Ghanim H; Dhindsa S; Abuaysheh S; Batra M; Kuhadiya ND; Makdissi A; Chaudhuri A; Dandona P
[Ad] Endereço:Division of Endocrinology, Diabetes and MetabolismState University of New York at Buffalo, Williamsville, New York, USA.
[Ti] Título:Diminished androgen and estrogen receptors and aromatase levels in hypogonadal diabetic men: reversal with testosterone.
[So] Source:Eur J Endocrinol;178(3):277-283, 2018 Mar.
[Is] ISSN:1479-683X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:AIMS: One-third of males with type 2 diabetes (T2DM) have hypogonadism, characterized by low total and free testosterone concentrations. We hypothesized that this condition is associated with a compensatory increase in the expression of androgen receptors (AR) and that testosterone replacement reverses these changes. We also measured estrogen receptor and aromatase expression. MATERIALS AND METHODS: This is a randomized double-blind placebo-controlled trial. Thirty-two hypogonadal and 32 eugonadal men with T2DM were recruited. Hypogonadal men were randomized to receive intramuscular testosterone or saline every 2 weeks for 22 weeks. We measured AR, ERα and aromatase expression in peripheral blood mononuclear cells (MNC), adipose tissue and skeletal muscle in hypogonadal and eugonadal males with T2DM at baseline and after 22 weeks of treatment in those with hypogonadism. RESULTS: The mRNA expression of and aromatase in adipose tissue from hypogonadal men was significantly lower as compared to eugonadal men, and it increased significantly to levels comparable to those in eugonadal patients with T2DM following testosterone treatment. mRNA expression was also significantly lower in MNC from hypogonadal patients compared to eugonadal T2DM patients. Testosterone administration in hypogonadal patients also restored mRNA and nuclear extract protein levels from MNC to that in eugonadal patients. In the skeletal muscle, AR mRNA and protein expression are lower in men with hypogonadism. Testosterone treatment restored AR expression levels to that comparable to levels in eugonadal men. CONCLUSIONS: We conclude that, contrary to our hypothesis, the expression of AR, ERα and aromatase is significantly diminished in hypogonadal men as compared to eugonadal men with type 2 diabetes. Following testosterone replacement, there is a reversal of these deficits.
[Mh] Termos MeSH primário: Androgênios/uso terapêutico
Aromatase/genética
Diabetes Mellitus Tipo 2/metabolismo
Receptor alfa de Estrogênio/genética
Hipogonadismo/tratamento farmacológico
Leucócitos Mononucleares/metabolismo
Receptores Androgênicos/genética
Testosterona/uso terapêutico
[Mh] Termos MeSH secundário: Adulto
Idoso
Aromatase/metabolismo
Western Blotting
Diabetes Mellitus Tipo 2/complicações
Método Duplo-Cego
Receptor alfa de Estrogênio/metabolismo
Seres Humanos
Hipogonadismo/complicações
Hipogonadismo/genética
Hipogonadismo/metabolismo
Masculino
Meia-Idade
RNA Mensageiro/metabolismo
Reação em Cadeia da Polimerase em Tempo Real
Receptores Androgênicos/metabolismo
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Gordura Subcutânea/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (AR protein, human); 0 (Androgens); 0 (Estrogen Receptor alpha); 0 (RNA, Messenger); 0 (Receptors, Androgen); 0 (estrogen receptor alpha, human); 3XMK78S47O (Testosterone); EC 1.14.14.1 (Aromatase); EC 1.14.14.1 (CYP19A1 protein, human)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180118
[St] Status:MEDLINE
[do] DOI:10.1530/EJE-17-0673


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[PMID]:29406096
[Au] Autor:Dong X; Zhang L; Chen M; Yang Z; Zuo Z; Wang C
[Ad] Endereço:State Key Laboratory of Cellular Stress Biology, School of Life Sciences, Xiamen University, Xiamen, China. Electronic address: 402127413@qq.com.
[Ti] Título:Exposure to difenoconazole inhibits reproductive ability in male marine medaka (Oryzias melastigma).
[So] Source:J Environ Sci (China);63:126-132, 2018 Jan.
[Is] ISSN:1001-0742
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Difenoconazole (DFZ) is a triazole fungicide which has been detected in the aquatic environment, including estuaries and embayments. However, few studies addressing the reproductive toxicity and transgenerational effects of DFZ on marine fishes are available. The present study was conducted to investigate the effects of DFZ on male marine medaka (Oryzias melastigma). After exposure of the embryo to 1, 10, 100 and 1000ng/L DFZ for 180days, the gonadosomatic index was significantly decreased in the 1000ng/L treatment. The number of sperm was reduced while the abundances of spermatocytes and spermatogonia in the testes were increased in all the treatments. The mRNA levels of salmon-type gnrh (sgnrh), the luteinizing hormone (lhß) and the follicle-stimulating hormone (fshß) genes in the brain all exhibited a significant down-regulation, the expression of androgen receptors (arα and arß) was decreased and that of estrogen receptor ß and cytochrome P450 aromatase (cyp19B) was increased in the testes. The expression levels of cyp19A and cyp19B were increased in the liver. The decrease of ars mRNA levels might be one of the reasons causing the reduction of sperm. The down-regulation of sgnrh, lhß and fshß mRNA levels suggested that DFZ might impact the spermatogenesis via the brain-pituitary-gonad pathway. The decrease of the fertilization success, the hatch ability and the swim-up success in the F1 generation indicated that DFZ pollution at environmental levels might cause a decrease of wild fish populations.
[Mh] Termos MeSH primário: Dioxolanos/toxicidade
Fungicidas Industriais/toxicidade
Oryzias/fisiologia
Triazóis/toxicidade
[Mh] Termos MeSH secundário: Animais
Aromatase/metabolismo
Masculino
Receptores Androgênicos
Reprodução/efeitos dos fármacos
Testículo
Poluentes Químicos da Água/toxicidade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Dioxolanes); 0 (Fungicides, Industrial); 0 (Receptors, Androgen); 0 (Triazoles); 0 (Water Pollutants, Chemical); D9612XCH4P (difenoconazole); EC 1.14.14.1 (Aromatase)
[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:180207
[St] Status:MEDLINE


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[PMID]:29037848
[Au] Autor:Guchhait R; Chatterjee A; Gupta S; Debnath M; Mukherjee D; Pramanick K
[Ad] Endereço:Integrative Biology Research Unit, Department of Life Sciences, Presidency University, 86/1, College Street, Kolkata 700073, India.
[Ti] Título:Molecular mechanism of mercury-induced reproductive impairments in banded gourami, Trichogaster fasciata.
[So] Source:Gen Comp Endocrinol;255:40-48, 2018 Jan 01.
[Is] ISSN:1095-6840
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Mercury is one of the key pollutants responsible for the degradation of natural aquatic ecosystems. Among the different forms of mercury that exist in the environment, mercuric chloride (HgCl ) is the dominant pollutant for freshwater environments as it is used as an ingredient in antiseptics, disinfectants and preservatives, insecticides, batteries and in metallurgical and photographic operations. Pollutant may exert their action on organisms or populations by affecting their normal endocrine function as well as reproduction. Thus, the present study tried to understand the effect of mercuric chloride (HgCl ) on reproductive function and to decipher the molecular mechanism of Hg-induced reproductive impairments of female Trichogaster fasciata. Both in vivo and in vitro experiments were performed by using ecologically relevant doses of HgCl and the resulting effects on follicular development, steroidogenic potentiality, aromatase activity, aromatase gene expression and steroidogenic factor-1 (SF-1) expression pattern were analysed. In vivo exposure to HgCl caused reproductive impairments as shown by the inhibitory role of HgCl on follicular development, steroid biosynthesis and SF-1 activity. In vitro experiments revealed that aromatase activity, steroidogenesis, aromatase and SF-1 expression were blocked by HgCl . The results obtained from this study contribute to understand the molecular mechanism of HgCl -induced reproductive impairment of T. fasciata.
[Mh] Termos MeSH primário: Peixes/fisiologia
Mercúrio/toxicidade
Reprodução/fisiologia
[Mh] Termos MeSH secundário: Animais
Aromatase/genética
Aromatase/metabolismo
Estradiol/biossíntese
Feminino
Regulação Enzimológica da Expressão Gênica/efeitos dos fármacos
Cloreto de Mercúrio/toxicidade
Folículo Ovariano/efeitos dos fármacos
Folículo Ovariano/enzimologia
Folículo Ovariano/crescimento & desenvolvimento
Reprodução/efeitos dos fármacos
Fator Esteroidogênico 1/metabolismo
Esteroides/biossíntese
Testosterona/biossíntese
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Steroidogenic Factor 1); 0 (Steroids); 3XMK78S47O (Testosterone); 4TI98Z838E (Estradiol); 53GH7MZT1R (Mercuric Chloride); EC 1.14.14.1 (Aromatase); FXS1BY2PGL (Mercury)
[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:171018
[St] Status:MEDLINE


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[PMID]:28578073
[Au] Autor:Baravalle R; Ciaramella A; Baj F; Di Nardo G; Gilardi G
[Ad] Endereço:Department of Life Sciences and Systems Biology, University of Torino, Via Accademia Albertina 13, Torino, Italy.
[Ti] Título:Identification of endocrine disrupting chemicals acting on human aromatase.
[So] Source:Biochim Biophys Acta;1866(1):88-96, 2018 01.
[Is] ISSN:0006-3002
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Human aromatase is the cytochrome P450 catalysing the conversion of androgens into estrogens playing a key role in the endocrine system. Due to this role, it is likely to be a target of the so-called endocrine disrupting chemicals, a series of compounds able to interfere with the hormone system with toxic effects. If on one side the toxicity of some compounds such as bisphenol A is well known, on the other side the toxic concentrations of such compounds as well as the effect of the many other molecules that are in contact with us in everyday life still need a deep investigation. The availability of biological assays able to detect the interaction of chemicals with key molecular targets of the endocrine system represents a possible solution to identify potential endocrine disrupting chemicals. Here the so-called alkali assay previously developed in our laboratory is applied to test the effect of different compounds on the activity of human aromatase. The assay is based on the detection of the alkali product that forms upon strong alkali treatment of the NADP released upon enzyme turnover. Here it is applied on human aromatase and validated using anastrozole and sildenafil as known aromatase inhibitors. Out of the small library of compounds tested, resveratrol and ketoconazole resulted to inhibit aromatase activity, while bisphenol A and nicotine were found to exert an inhibitory effect at relatively high concentrations (100µM), and other molecules such as lindane and four plasticizers did not show any significant effect. These data are confirmed by quantification of the product estrone in the same reaction mixtures through ELISA. Overall, the results show that the alkali assay is suitable to screen for molecules that interfere with aromatase activity. As a consequence it can also be applied to other molecular targets of EDCs that use NAD(P)H for catalysis in a high throughput format for the fast screening of many different compounds as endocrine disrupting chemicals. This article is part of a Special Issue entitled: Cytochrome P450 biodiversity and biotechnology, edited by Erika Plettner, Gianfranco Gilardi, Luet Wong, Vlada Urlacher, Jared Goldstone.
[Mh] Termos MeSH primário: Inibidores da Aromatase/química
Aromatase/química
Bioensaio
Disruptores Endócrinos/química
[Mh] Termos MeSH secundário: Aromatase/genética
Inibidores da Aromatase/análise
Compostos Benzidrílicos/análise
Compostos Benzidrílicos/química
Disruptores Endócrinos/análise
Ensaio de Imunoadsorção Enzimática
Estrona/química
Expressão Gênica
Seres Humanos
Cetoconazol/análise
Cetoconazol/química
Ligantes
NADP/química
Nicotina/análise
Nicotina/química
Nitrilos/análise
Nitrilos/química
Fenóis/análise
Fenóis/química
Ligação Proteica
Proteínas Recombinantes/química
Proteínas Recombinantes/genética
Citrato de Sildenafila/análise
Citrato de Sildenafila/química
Bibliotecas de Moléculas Pequenas/análise
Bibliotecas de Moléculas Pequenas/química
Estilbenos/análise
Estilbenos/química
Triazóis/análise
Triazóis/química
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Aromatase Inhibitors); 0 (Benzhydryl Compounds); 0 (Endocrine Disruptors); 0 (Ligands); 0 (Nitriles); 0 (Phenols); 0 (Recombinant Proteins); 0 (Small Molecule Libraries); 0 (Stilbenes); 0 (Triazoles); 2DI9HA706A (Estrone); 2Z07MYW1AZ (anastrozole); 53-59-8 (NADP); 6M3C89ZY6R (Nicotine); BW9B0ZE037 (Sildenafil Citrate); EC 1.14.14.1 (Aromatase); EC 1.14.14.1 (CYP19A1 protein, human); MLT3645I99 (bisphenol A); Q369O8926L (resveratrol); R9400W927I (Ketoconazole)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180208
[Lr] Data última revisão:
180208
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170605
[St] Status:MEDLINE


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[PMID]:28452938
[Au] Autor:Casarini L; Riccetti L; De Pascali F; Gilioli L; Marino M; Vecchi E; Morini D; Nicoli A; La Sala GB; Simoni M
[Ad] Endereço:Unit of Endocrinology, Department of Biomedical, Metabolic and Neural Sciences, University of Modena and Reggio Emilia, NOCSAE, via P. Giardini 1355, 41126 Modena, Italy. livio.casarini@unimore.it.
[Ti] Título:Estrogen Modulates Specific Life and Death Signals Induced by LH and hCG in Human Primary Granulosa Cells In Vitro.
[So] Source:Int J Mol Sci;18(5), 2017 Apr 28.
[Is] ISSN:1422-0067
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Luteinizing hormone (LH) and human chorionic gonadotropin (hCG) are glycoprotein hormones used for assisted reproduction acting on the same receptor (LHCGR) and mediating different intracellular signaling. We evaluated the pro- and anti-apoptotic effect of 100 pM LH or hCG, in the presence or in the absence of 200 pg/mL 17ß-estradiol, in long-term, serum-starved human primary granulosa cells (hGLC) and a transfected granulosa cell line overexpressing LHCGR (hGL5/LHCGR). To this purpose, phospho-extracellular-regulated kinase 1/2 (pERK1/2), protein kinase B (pAKT), cAMP-responsive element binding protein (pCREB) activation and procaspase 3 cleavage were evaluated over three days by Western blotting, along with the expression of target genes by real-time PCR and cell viability by colorimetric assay. We found that LH induced predominant pERK1/2 and pAKT activation , and anti-apoptotic gene expression, while hCG mediated more potent CREB phosphorylation, expression of and procaspase 3 cleavage than LH. Cell treatment by LH is accompanied by increased (serum-starved) cell viability, while hCG decreased the number of viable cells. The hCG-specific, pro-apoptotic effect was blocked by a physiological dose of 17ß-estradiol, resulting in pAKT activation, lack of procaspase 3 cleavage and increased cell viability. These results confirm that relatively high levels of steroidogenic pathway activation are linked to pro-apoptotic signals in vitro, which may be counteracted by other factors, i.e., estrogens.
[Mh] Termos MeSH primário: Gonadotropina Coriônica/farmacologia
Estradiol/farmacologia
Hormônio Luteinizante/farmacologia
Transdução de Sinais/efeitos dos fármacos
[Mh] Termos MeSH secundário: Aromatase/metabolismo
Proteína de Ligação a CREB/metabolismo
Caspase 3/genética
Caspase 3/metabolismo
Sobrevivência Celular/efeitos dos fármacos
Células Cultivadas
Feminino
Expressão Gênica/efeitos dos fármacos
Células da Granulosa/citologia
Células da Granulosa/efeitos dos fármacos
Células da Granulosa/metabolismo
Seres Humanos
Proteína Quinase 1 Ativada por Mitógeno/metabolismo
Proteína Quinase 3 Ativada por Mitógeno/metabolismo
Fosforilação/efeitos dos fármacos
Proteínas Proto-Oncogênicas c-akt/metabolismo
Proteína Supressora de Tumor p53/genética
Proteína Supressora de Tumor p53/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chorionic Gonadotropin); 0 (Tumor Suppressor Protein p53); 4TI98Z838E (Estradiol); 9002-67-9 (Luteinizing Hormone); EC 1.14.14.1 (Aromatase); EC 1.14.14.1 (CYP19A1 protein, human); EC 2.3.1.48 (CREB-Binding Protein); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 1); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 3); EC 3.4.22.- (Caspase 3)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180122
[Lr] Data última revisão:
180122
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE


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[PMID]:28448463
[Au] Autor:Atta MS; Almadaly EA; El-Far AH; Saleh RM; Assar DH; Al Jaouni SK; Mousa SA
[Ad] Endereço:Department of Physiology, Faculty of Veterinary Medicine, Kafrelsheikh University, Kafrelsheikh 33516, Egypt. mostafa.ataa@vet.kfs.edu.eg.
[Ti] Título:Thymoquinone Defeats Diabetes-Induced Testicular Damage in Rats Targeting Antioxidant, Inflammatory and Aromatase Expression.
[So] Source:Int J Mol Sci;18(5), 2017 Apr 27.
[Is] ISSN:1422-0067
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Antioxidants have valuable effects on the process of spermatogenesis, particularly with diabetes mellitus (DM). Therefore, the present study investigated the impact and the intracellular mechanisms by which thymoquinone (TQ) works against diabetes-induced testicular deteriorations in rats. Wistar male rats ( = 60) were randomly allocated into four groups; Control, Diabetic (streptozotocin (STZ)-treated rats where diabetes was induced by intraperitoneal injection of STZ, 65 mg/kg), Diabetic + TQ (diabetic rats treated with TQ (50 mg/kg) orally once daily), and TQ (non-diabetic rats treated with TQ) for 12 weeks. Results revealed that TQ significantly improved the sperm parameters with a reduction in nitric oxide (NO) and malondialdehyde (MDA) levels in testicular tissue. Also, it increased testicular reduced glutathione (GSH) levels and superoxide dismutase (SOD) activity. Interestingly, TQ induced downregulation of testicular inducible nitric oxide synthase (iNOS) and nuclear factor kappa-B (NF-κB) and significantly upregulated the aromatase protein expression levels in testicles in comparison with the diabetic rats. In conclusion, TQ treatment exerted a protective effect against reproductive dysfunction induced by diabetes not only through its powerful antioxidant and hypoglycemic effects but also through its downregulation of testicular iNOS and NF-κB along with upregulation of aromatase expression levels in diabetic rats.
[Mh] Termos MeSH primário: Antioxidantes/metabolismo
Aromatase/metabolismo
Benzoquinonas/farmacologia
Substâncias Protetoras/farmacologia
Espermatogênese/efeitos dos fármacos
Testículo/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Peso Corporal/efeitos dos fármacos
Diabetes Mellitus Experimental/induzido quimicamente
Diabetes Mellitus Experimental/patologia
Glutationa/metabolismo
Masculino
Malondialdeído/metabolismo
NF-kappa B/metabolismo
Óxido Nítrico/metabolismo
Óxido Nítrico Sintase Tipo II/metabolismo
Estresse Oxidativo/efeitos dos fármacos
Ratos
Ratos Wistar
Estreptozocina/toxicidade
Superóxido Dismutase/metabolismo
Testículo/metabolismo
Testículo/patologia
Regulação para Cima/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antioxidants); 0 (Benzoquinones); 0 (NF-kappa B); 0 (Protective Agents); 31C4KY9ESH (Nitric Oxide); 490-91-5 (thymoquinone); 4Y8F71G49Q (Malondialdehyde); 5W494URQ81 (Streptozocin); EC 1.14.13.39 (Nitric Oxide Synthase Type II); EC 1.14.14.1 (Aromatase); EC 1.15.1.1 (Superoxide Dismutase); GAN16C9B8O (Glutathione)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180122
[Lr] Data última revisão:
180122
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170428
[St] Status:MEDLINE


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[PMID]:27773742
[Au] Autor:Mahalingam S; Gao L; Eisner J; Helferich W; Flaws JA
[Ad] Endereço:Department of Comparative Biosciences, College of Veterinary Medicine, University of Illinois, 2001 S. Lincoln Ave, Urbana, IL 61802, United States. Electronic address: mahalin2@illinois.edu.
[Ti] Título:Effects of isoliquiritigenin on ovarian antral follicle growth and steroidogenesis.
[So] Source:Reprod Toxicol;66:107-114, 2016 12.
[Is] ISSN:1873-1708
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Isoliquiritigenin is a botanical estrogen used as a dietary supplement. Previous studies show that other botanical estrogens affect ovarian estradiol synthesis, but isoliquiritigenin's effects on the ovary are unknown. Thus, this study tested the hypothesis that isoliquiritigenin inhibits ovarian antral follicle growth and steroidogenesis. Antral follicles from CD-1 mice were cultured with vehicle control (dimethyl sulfoxide; DMSO) or isoliquiritigenin (0.6µM, 6 µM, 36 µM, and 100 µM) for 48-96h. During culture, follicle diameters were measured daily to assess follicle growth. After culture, media were collected for hormone assays and follicles were collected for gene expression analysis of steroidogenic enzymes. Isoliquiritigenin inhibited antral follicle growth and altered estradiol, testosterone, and progesterone levels. Additionally, isoliquiritigenin altered the mRNA levels of cytochrome P450 steroid 17-α-hydroxylase 1, aromatase, 17ß-hydroxysteroid dehydrogenase 1, and steroidogenic acute regulatory protein. These data indicate that exposure to isoliquiritigenin inhibits growth and disrupts steroid production in antral follicles.
[Mh] Termos MeSH primário: Chalconas/toxicidade
Folículo Ovariano/efeitos dos fármacos
[Mh] Termos MeSH secundário: 17-Hidroxiesteroide Desidrogenases/genética
Animais
Aromatase/genética
Estradiol/metabolismo
Feminino
Camundongos
Folículo Ovariano/crescimento & desenvolvimento
Folículo Ovariano/metabolismo
Fosfoproteínas/genética
Progesterona/metabolismo
RNA Mensageiro/metabolismo
Esteroide 17-alfa-Hidroxilase/genética
Testosterona/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Chalcones); 0 (Phosphoproteins); 0 (RNA, Messenger); 0 (steroidogenic acute regulatory protein); 3XMK78S47O (Testosterone); 4G7DS2Q64Y (Progesterone); 4TI98Z838E (Estradiol); B9CTI9GB8F (isoliquiritigenin); EC 1.1.- (17-Hydroxysteroid Dehydrogenases); EC 1.1.- (hydroxysteroid (17-beta) dehydrogenase 1, mouse); EC 1.14.14.1 (Aromatase); EC 1.14.14.19 (Steroid 17-alpha-Hydroxylase)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180113
[Lr] Data última revisão:
180113
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE


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[PMID]:29202405
[Au] Autor:Kang H; Xiao X; Huang C; Yuan Y; Tang D; Dai X; Zeng X
[Ad] Endereço:Key Laboratory of Medicinal Chemistry for Natural Resource, Ministry of Education, School of Chemical Science and Technology, Yunnan University, Kunming 650091, PR China.
[Ti] Título:Potent aromatase inhibitors and molecular mechanism of inhibitory action.
[So] Source:Eur J Med Chem;143:426-437, 2018 Jan 01.
[Is] ISSN:1768-3254
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:Estrogen is a significant factor in the maintenance and progression of hormone-dependent breast cancer. As well known, aromatase mediates the production of estrogen. Thus, inhibition of aromatase with chemical molecules has been considered to be an effective treatment for estrogen receptor-positive (ER+) breast cancer. In this work, we designed and synthesized a series of novel non-steroidal molecules containing 2-phenylindole scaffold and moiety of either imidazole or 1,2,4-triazole to enhance their binding capacity with the aromatase. Among these molecules, a compound named as 8o was confirmed experimentally to have the highest inhibitory activity to aromatase. Further cell activity assay proved that compound 8o has low cytotoxicity and is a promising lead for developing novel aromatase inhibitors. Molecular modeling and simulation techniques were performed to identify the binding modes of letrozole and 8o with the aromatase. Analysis of energy of the two compound-aromatase complexes revealed that the 8o has low binding energy (strong binding affinity) to the aromatase as compared to letrozole, which was in accordance with the experimental results. As concluded, a combination of experimental and computational approaches facilitates us to understand the molecular mechanism of inhibitory action and discover more potent non-steroidal AIs against aromatase, thereby opening up a novel therapeutic strategy for hormone-dependent breast cancer.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Inibidores da Aromatase/farmacologia
Aromatase/metabolismo
[Mh] Termos MeSH secundário: Antineoplásicos/síntese química
Antineoplásicos/química
Inibidores da Aromatase/síntese química
Inibidores da Aromatase/química
Proliferação Celular/efeitos dos fármacos
Relação Dose-Resposta a Droga
Ensaios de Seleção de Medicamentos Antitumorais
Seres Humanos
Células MCF-7
Modelos Moleculares
Estrutura Molecular
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Aromatase Inhibitors); EC 1.14.14.1 (Aromatase); EC 1.14.14.1 (CYP19A1 protein, human)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180101
[Lr] Data última revisão:
180101
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171205
[St] Status:MEDLINE


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[PMID]:27776294
[Au] Autor:Desautels DN; Blanchette PS; Pritchard KI
[Ad] Endereço:Division of Medical Oncology, University of Toronto, Toronto, Ontario, Canada.
[Ti] Título:Do aromatase inhibitors increase cardiovascular risk? Piecing together the evidence.
[So] Source:Eur J Cancer;68:176-178, 2016 11.
[Is] ISSN:1879-0852
[Cp] País de publicação:England
[La] Idioma:eng
[Mh] Termos MeSH primário: Inibidores da Aromatase
Doenças Cardiovasculares
[Mh] Termos MeSH secundário: Aromatase
Neoplasias da Mama
Inibidores Enzimáticos
Seres Humanos
Fatores de Risco
[Pt] Tipo de publicação:EDITORIAL; COMMENT
[Nm] Nome de substância:
0 (Aromatase Inhibitors); 0 (Enzyme Inhibitors); EC 1.14.14.1 (Aromatase)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180101
[Lr] Data última revisão:
180101
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE



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