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[PMID]:25517940
[Au] Autor:Dimri M; Joshi J; Chakrabarti R; Sehgal N; Sureshbabu A; Kumar IP
[Ad] Endereço:1 Radiation Biosciences Division, Institute of Nuclear Medicine and Allied Sciences , Defense Research and Development Organization, Delhi, India .
[Ti] Título:Todralazine protects zebrafish from lethal effects of ionizing radiation: role of hematopoietic cell expansion.
[So] Source:Zebrafish;12(1):33-47, 2015 Feb.
[Is] ISSN:1557-8542
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The Johns Hopkins Clinical Compound Library (JHCCL), a collection of Food and Drug Administration (FDA)-approved small molecules (1400), was screened in silico for identification of novel ß2AR blockers and tested for hematopoietic stem cell (HSC) expansion and radioprotection in zebrafish embryos. Docking studies, followed by the capacity to hasten erythropoiesis, identified todralazine (Binding energy, -8.4 kcal/mol) as a potential HSC-modulating agent. Todralazine (5 µM) significantly increased erythropoiesis in caudal hematopoietic tissue (CHT) in wild-type and anemic zebrafish embryos (2.33- and 1.44-folds, respectively) when compared with untreated and anemic control groups. Todralazine (5 µM) treatment also led to an increased number of erythroid progenitors, as revealed from the increased expression of erythroid progenitor-specific genes in the CHT region. Consistent with these effects, zebrafish embryos, Tg(cmyb:gfp), treated with 5 µM todralazine from 24 to 36 hours post fertilization (hpf) showed increased (approximately two-folds) number of HSCs at the aorta-gonad-mesonephros region (AGM). Similarly, expression of HSC marker genes, runx1 (3.3-folds), and cMyb (1.41-folds) also increased in case of todralazine-treated embryos, further supporting its HSC expansion potential. Metoprolol, a known beta blocker, also induced HSC expansion (1.36- and 1.48-fold increase in runx1 and cMyb, respectively). Todralazine (5 µM) when added 30 min before 20 Gy gamma radiation, protected zebrafish from radiation-induced organ toxicity, apoptosis, and improved survival (80% survival advantage over 6 days). The 2-deoxyribose degradation test further suggested hydroxyl (OH) radical scavenging potential of todralazine, and the same is recapitulated in vivo. These results suggest that todralazine is a potential HSC expanding agent, which might be acting along with important functions, such as antioxidant and free radical scavenging, in manifesting radioprotection.
[Mh] Termos MeSH primário: Antagonistas de Receptores Adrenérgicos beta 2/farmacologia
Células-Tronco Hematopoéticas/efeitos dos fármacos
Radiação Ionizante
Todralazina/farmacologia
Peixe-Zebra/metabolismo
[Mh] Termos MeSH secundário: Animais
Embrião não Mamífero/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Adrenergic beta-2 Receptor Antagonists); WEN3K83YKD (Todralazine)
[Em] Mês de entrada:1509
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:141218
[St] Status:MEDLINE
[do] DOI:10.1089/zeb.2014.0992


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[PMID]:17161489
[Au] Autor:Elsharkawy AM
[Ti] Título:Todralazine hepatotoxicity: a sting in the histone tail.
[So] Source:J Hepatol;46(2):189-92, 2007 Feb.
[Is] ISSN:0168-8278
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Mh] Termos MeSH primário: Anti-Hipertensivos/toxicidade
Histonas/efeitos dos fármacos
Falência Hepática/induzido quimicamente
Fígado/efeitos dos fármacos
Todralazina/toxicidade
[Mh] Termos MeSH secundário: Acetilação/efeitos dos fármacos
Animais
Anti-Hipertensivos/efeitos adversos
Histonas/metabolismo
Seres Humanos
Fígado/metabolismo
Falência Hepática/metabolismo
Camundongos
Todralazina/efeitos adversos
[Pt] Tipo de publicação:COMMENT; EDITORIAL
[Nm] Nome de substância:
0 (Antihypertensive Agents); 0 (Histones); WEN3K83YKD (Todralazine)
[Em] Mês de entrada:0703
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:061213
[St] Status:MEDLINE


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[PMID]:17156885
[Au] Autor:Murata K; Hamada M; Sugimoto K; Nakano T
[Ad] Endereço:First Department of Internal Medicine, Mie University School of Medicine, 2-174 Edobashi, Tsu, Mie 514-8507, Japan. atarum@clin.medic.mie-u.ac.jp
[Ti] Título:A novel mechanism for drug-induced liver failure: inhibition of histone acetylation by hydralazine derivatives.
[So] Source:J Hepatol;46(2):322-9, 2007 Feb.
[Is] ISSN:0168-8278
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: The aim of this study was to investigate the precise mechanism of liver failure by hydralazine derivatives, with special reference to liver regeneration failure. METHODS: Histone acetylation and proliferation of hepatocytes were evaluated by immunohistochemistry with anti-acetylated histone H4 and proliferating cell nuclear antigen (PCNA). Inhibition of histone acetylation by drugs was determined by in vitro histone acetylation assay. Mice livers fed with todralazine for 1 or 4 months were subjected to immunohistochemistry and Western blotting. Todralazine-fed mice were challenged with anti-Fas to check liver regeneration failure. RESULTS: On immunohistochemistry, histone acetylation in the hepatocytes was significantly impaired in patients with hydralazine derivatives. In an in vitro acetyl transferase assay, histone acetylation was inhibited by hydralazine derivatives in a dose-dependent manner. Mice fed with todralazine (3mg/day) for 4 months showed impairment of histone acetylation in hepatocytes whereas no inhibition was observed in mice fed with todralazine for 1 month. Anti-Fas challenge to todralazine-fed mice resulted in impairment of liver regeneration in respect of liver weight loss with impairment of histone acetylation in hepatocytes. CONCLUSIONS: Todralazine could inhibit catalysis of histone acetyltransferase and long-term administration of todralazine may impair histone acetylation of the hepatocytes, resulting in liver regeneration failure.
[Mh] Termos MeSH primário: Histonas/antagonistas & inibidores
Hidralazina/análogos & derivados
Falência Hepática/induzido quimicamente
Falência Hepática/metabolismo
Todralazina/toxicidade
[Mh] Termos MeSH secundário: Acetilação/efeitos dos fármacos
Acetiltransferases/análise
Animais
Arilamina N-Acetiltransferase/genética
Modelos Animais de Doenças
Feminino
Histonas/metabolismo
Seres Humanos
Fígado/efeitos dos fármacos
Fígado/metabolismo
Fígado/patologia
Falência Hepática/patologia
Regeneração Hepática/efeitos dos fármacos
Camundongos
Receptor fas/antagonistas & inibidores
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Histones); 0 (fas Receptor); 26NAK24LS8 (Hydralazine); EC 2.3.1.- (Acetyltransferases); EC 2.3.1.5 (Arylamine N-Acetyltransferase); EC 2.3.1.5 (NAT2 protein, human); WEN3K83YKD (Todralazine)
[Em] Mês de entrada:0703
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:061213
[St] Status:MEDLINE


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[PMID]:11753436
[Au] Autor:Gasiorowski K; Brokos B
[Ad] Endereço:Wroclaw Medical University, Department of Basic Medical Sciences, Kochanowskiego 14, 51-601 Wroclaw, Poland. kaz@basmed.am.wroc.pl
[Ti] Título:DNA repair of hydrogen peroxide-induced damage in human lymphocytes in the presence of four antimutagens. A study with alkaline single cell gel electrophoresis (comet assay).
[So] Source:Cell Mol Biol Lett;6(4):897-911, 2001.
[Is] ISSN:1425-8153
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:We assessed four antimutagenic compounds' influences on DNA repair in human lymphocytes exposed in vitro to hydrogen peroxide (20 microM, 5 min, at 4 degrees C). DNA damage and repair were estimated by means of alkaline single cell gel electrophoresis (comet assay). It was noticed that the enhancement of DNA repair was relatively strongest when fluphenazine was present in the cell culture medium. In the cases of anthocyanins and alkylresorcinols, the effects were almost 6-9 times weaker than that of FPh. The effect of todralazine on DNA repair was relatively weakest. Further study should be done on fluphenazine as a potential DNA repair-enhancing compound.
[Mh] Termos MeSH primário: Antimutagênicos/farmacologia
Reparo do DNA/efeitos dos fármacos
Peróxido de Hidrogênio/toxicidade
Linfócitos/efeitos dos fármacos
Linfócitos/metabolismo
[Mh] Termos MeSH secundário: Adulto
Antocianinas/farmacologia
Ensaio Cometa
Dano ao DNA
Flufenazina/farmacologia
Seres Humanos
Técnicas In Vitro
Masculino
Meia-Idade
Resorcinóis/farmacologia
Todralazina/farmacologia
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anthocyanins); 0 (Antimutagenic Agents); 0 (Resorcinols); BBX060AN9V (Hydrogen Peroxide); S79426A41Z (Fluphenazine); WEN3K83YKD (Todralazine)
[Em] Mês de entrada:0203
[Cu] Atualização por classe:141120
[Lr] Data última revisão:
141120
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:011226
[St] Status:MEDLINE


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[PMID]:10719039
[Au] Autor:Gasiorowski K; Brokos B
[Ad] Endereço:Wroclaw Medical University, Department of Basic Medical Sciences, 14 Kochanowskiego Str., 51-01 Wroclaw, Poland. kaz@basmed.am.wroc.pl
[Ti] Título:Evaluation of antimutagenic effect of todralazine in cultured lymphocytes.
[So] Source:Mutagenesis;15(2):137-41, 2000 Mar.
[Is] ISSN:0267-8357
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Todralazine, an antihypertensive drug from the hydrazinophthalazine group, significantly decreased the activities of benzo[a]pyrene and mitomycin C in three short-term genotoxicity tests in human lymphocyte cultures. The thioguanine resistance test, the cytokinesis-blocked micronucleus assay and the sister chromatid exchange test were used to demonstrate the antimutagenicity of todralazine. Todralazine lowered the level of free radicals generated by human granulocytes in vitro in the presence of benzo[a] pyrene and also in the presence of the granulocyte activator and tumor promoter phorbol myristate acetate. These results, together with our previous data obtained in the standard bacterial Ames test, strongly suggest that todralazine is a good antimutagen in vitro and deserves further research on its inhibitory action on mutagenesis and carcinogenesis.
[Mh] Termos MeSH primário: Antimutagênicos/farmacologia
Todralazina/farmacologia
[Mh] Termos MeSH secundário: Adulto
Divisão Celular/efeitos dos fármacos
Células Cultivadas
Relação Dose-Resposta a Droga
Radicais Livres
Granulócitos/efeitos dos fármacos
Seres Humanos
Linfócitos/efeitos dos fármacos
Masculino
Micronúcleos com Defeito Cromossômico/efeitos dos fármacos
Meia-Idade
Testes de Mutagenicidade
Troca de Cromátide Irmã/efeitos dos fármacos
Fumar
Tioguanina/metabolismo
Todralazina/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antimutagenic Agents); 0 (Free Radicals); FTK8U1GZNX (Thioguanine); WEN3K83YKD (Todralazine)
[Em] Mês de entrada:0005
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:000317
[St] Status:MEDLINE


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[PMID]:9412993
[Au] Autor:Gasiorowski K; Szyba K; Wozniak D; Gulanowski B
[Ad] Endereço:Medical University, Department of Basic Medical Sciences, Wroclaw, Poland.
[Ti] Título:Inhibition of potassium dichromate mutagenicity by todralazine.
[So] Source:Mutagenesis;12(6):411-5, 1997 Nov.
[Is] ISSN:0267-8357
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Todralazine, an antihypertensive drug of the hydrazinoph-thalazine group, markedly decreased the mutagenic activity of potassium dichromate in standard bacterial tests. At the highest todralazine dose tested inhibition of potassium dichromate mutagenic activity by approximately 90% in the Ames test and up to 100% (complete) inhibition in the Bacillus subtilis rec- assay was observed. Spectrophotometric analyses proved that todralazine induced reduction of Cr(VI) to Cr(III) and complexation of Cr(III) ions. These spectro-photometric results may be a presumptive explanation of the observed mutagenic activity decrease, as it is known that Cr(III) is poorly transported across cell membranes and therefore is not mutagenic to bacterial cells. We perceive our experiments as an example of attempts which should lead to an effective reduction in chromium genotoxic and carcinogenic activity in exposed individuals.
[Mh] Termos MeSH primário: Anti-Hipertensivos/farmacologia
Cáusticos/toxicidade
Mutagênicos/toxicidade
Dicromato de Potássio/antagonistas & inibidores
Dicromato de Potássio/toxicidade
Todralazina/farmacologia
[Mh] Termos MeSH secundário: Antimutagênicos/farmacologia
Bacillus subtilis/efeitos dos fármacos
Relação Dose-Resposta a Droga
Mutagênese/efeitos dos fármacos
Testes de Mutagenicidade
Dicromato de Potássio/química
Análise de Regressão
Salmonella typhimurium/efeitos dos fármacos
Espectrofotometria
Todralazina/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antihypertensive Agents); 0 (Antimutagenic Agents); 0 (Caustics); 0 (Mutagens); T4423S18FM (Potassium Dichromate); WEN3K83YKD (Todralazine)
[Em] Mês de entrada:9802
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:971231
[St] Status:MEDLINE


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[PMID]:9415211
[Au] Autor:Chlopkiewicz B
[Ad] Endereço:Drug Institute, Warsaw, Poland.
[Ti] Título:Genotoxicity of hydrazino-phtalazine antihypertensive drugs assessed by an in vitro micronucleus assay.
[So] Source:Acta Pol Pharm;53(5):361-4, 1996 Sep-Oct.
[Is] ISSN:0001-6837
[Cp] País de publicação:Poland
[La] Idioma:eng
[Ab] Resumo:The genotoxicity of antihypertensive drugs, hydralazine, dihydralazine and binazine was assessed on the base of their capacity to induce micronuclei in L929 cell line. In our previous investigations we indicated that these drugs did not induce micronuclei in bone marrow polichromatic erythrocytes in PZH SFISS mice. Present results show that hydralazine and dihydralizine can induce micronuclei in vitro and that this effect depends on time of exposure and the concentration of drug.
[Mh] Termos MeSH primário: Anti-Hipertensivos/toxicidade
Di-Hidralazina/toxicidade
Hidralazina/toxicidade
Todralazina/toxicidade
[Mh] Termos MeSH secundário: Animais
Linhagem Celular/efeitos dos fármacos
Camundongos
Testes para Micronúcleos
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antihypertensive Agents); 26NAK24LS8 (Hydralazine); PCU411F5L6 (Dihydralazine); WEN3K83YKD (Todralazine)
[Em] Mês de entrada:9801
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:960901
[St] Status:MEDLINE


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[PMID]:8675265
[Au] Autor:Dohi Y; Kojima M; Sato K
[Ad] Endereço:Second Department of Internal Medicine, Nagoya City University Hospital, Japan.
[Ti] Título:Benidipine improves endothelial function in renal resistance arteries of hypertensive rats.
[So] Source:Hypertension;28(1):58-63, 1996 Jul.
[Is] ISSN:0194-911X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We studied the effects of long-term antihypertensive treatment on endothelial function in renal resistance arteries from spontaneously hypertensive rats (SHR). Wistar-Kyoto rats (WKY) were used as a normotensive reference. Adult SHR were treated with benidipine (a calcium antagonist) or ecarazine (a vasodilator) for 10 weeks; the drugs caused similar reductions in blood pressure. Changes in isometric tension of rings prepared from the third-order branches of the renal arteries were recorded. Endothelium-dependent relaxations induced by acetylcholine in rings contracted with norepinephrine were smaller in SHR than in WKY. The impaired relaxation was improved by benidipine treatment, but ecarazine had no significant effect. In vitro treatment with meclofenamic acid, a cyclooxygenase inhibitor, did not alter the differences in the relaxations. In the presence of meclofenamic acid, N omega-nitro-L-arginine methyl ester slightly reduced the relaxations; the relaxation was smaller in SHR than in WKY and was not affected by benidipine treatment. In rings contracted with 40 mmol/L. KCI, the relaxations induced by acetylcholine in the presence of meclofenamic acid were smaller than those in rings contracted with norepinephrine. The relaxation was smaller in SHR than in WKY but was normalized by benidipine treatment. Thus, acetylcholine relaxes rat renal resistance arteries by releasing nitric oxide and endothelium-derived hyperpolarizing factor from the endothelium, which is impaired in SHR. Long-term benidipine treatment improves the impaired relaxation in SHR by enhancing nitric oxide-mediated relaxation.
[Mh] Termos MeSH primário: Bloqueadores dos Canais de Cálcio/farmacologia
Di-Hidropiridinas/farmacologia
Endotélio Vascular/efeitos dos fármacos
Hipertensão/tratamento farmacológico
Artéria Renal/efeitos dos fármacos
[Mh] Termos MeSH secundário: Acetilcolina/farmacologia
Animais
Anti-Hipertensivos/administração & dosagem
Anti-Hipertensivos/farmacologia
Anti-Hipertensivos/uso terapêutico
Pressão Sanguínea/efeitos dos fármacos
Bloqueadores dos Canais de Cálcio/administração & dosagem
Bloqueadores dos Canais de Cálcio/uso terapêutico
Di-Hidropiridinas/administração & dosagem
Di-Hidropiridinas/uso terapêutico
Endotélio Vascular/metabolismo
Endotélio Vascular/fisiopatologia
Frequência Cardíaca/efeitos dos fármacos
Hipertensão/fisiopatologia
Técnicas In Vitro
Masculino
Relaxamento Muscular/efeitos dos fármacos
Óxido Nítrico/metabolismo
Óxido Nítrico/fisiologia
Ratos
Ratos Endogâmicos SHR
Ratos Endogâmicos WKY
Artéria Renal/fisiopatologia
Fatores de Tempo
Todralazina/administração & dosagem
Todralazina/farmacologia
Todralazina/uso terapêutico
Resistência Vascular
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antihypertensive Agents); 0 (Calcium Channel Blockers); 0 (Dihydropyridines); 31C4KY9ESH (Nitric Oxide); 4G9T91JS7E (benidipine); N9YNS0M02X (Acetylcholine); WEN3K83YKD (Todralazine)
[Em] Mês de entrada:9608
[Cu] Atualização por classe:160726
[Lr] Data última revisão:
160726
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:960701
[St] Status:MEDLINE


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[PMID]:8617425
[Au] Autor:Tameda Y; Hamada M; Takase K; Nakano T; Kosaka Y
[Ad] Endereço:Department of Laboratory Medicine, Mie University, School of Medicine, Tsu, Japan.
[Ti] Título:Fulminant hepatic failure caused by ecarazine hydrochloride (a hydralazine derivative).
[So] Source:Hepatology;23(3):465-70, 1996 Mar.
[Is] ISSN:0270-9139
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The cause of fulminant hepatic failure is reported to be unknown in more than half the cases in Japan. We recently reviewed 23 cases of fulminant hepatic failure that had been treated at our hospital. The cause of disease had been regarded as unknown before this study. It was found that seven of these patients had been under ecarazine hydrochloride therapy when they developed fulminant hepatic failure. We examined the reasons why fulminant hepatic failure in these seven patients had not been previously attributed to ecarazine, and found that it could be explained by the following factors: (1) the time from the start of ecarazine therapy to the onset of hepatic failure was long; (2) in all cases, hepatic failure developed more than 10 days after the clinical recognition of hepatitis; and (3) characteristic signs of drug-induced hepatic failure such as a skin rash and positive lymphocytes stimulation test with the drug were absent in all cases. Fulminant hepatic failure in these cases could be characterized by: (1) rapid decrease in serum alanine transaminase (ALT) level after discontinuation of ecarazine, (2) prolonged jaundice despite discontinuation of ecarazine, (3) high incidence of anti-nuclear antibody (ANA) (57%), and (4) histological findings of extensive hepatocellular necrosis ranging from bridging necrosis to massive necrosis. Of the seven patients, four died of fulminant hepatic failure. These four patients had received high doses of ecarazine hydrochloride for prolonged periods. Our data suggest that there may be many cases in which the cause of fulminant hepatic failure or acute hepatitis was not previously determined that can be attributed to long-term drug therapy for chronic diseases.
[Mh] Termos MeSH primário: Anti-Hipertensivos/efeitos adversos
Encefalopatia Hepática/induzido quimicamente
Todralazina/efeitos adversos
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Alanina Transaminase/sangue
Anticorpos Antinucleares/sangue
Feminino
Encefalopatia Hepática/imunologia
Encefalopatia Hepática/patologia
Seres Humanos
Icterícia/etiologia
Fígado/enzimologia
Fígado/patologia
Masculino
Meia-Idade
Necrose
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies, Antinuclear); 0 (Antihypertensive Agents); EC 2.6.1.2 (Alanine Transaminase); WEN3K83YKD (Todralazine)
[Em] Mês de entrada:9606
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:960301
[St] Status:MEDLINE


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[PMID]:8960236
[Au] Autor:Chlopkiewicz B; Ejchart A; Marczewska J
[Ad] Endereço:Drug Institute, Warsaw, Poland.
[Ti] Título:Genetic effects of binazine and hydralazine in vitro and in vivo.
[So] Source:Acta Pol Pharm;52(1):31-3, 1995 Jan-Feb.
[Is] ISSN:0001-6837
[Cp] País de publicação:Poland
[La] Idioma:eng
[Ab] Resumo:The mutagenic and genotoxic activities of binazine and hydralazine were studied. In the Ames test, both with and without S-9 fraction, hydralazine was mutagenic in strains Salmonella typhimurium TA100 and TA1537, whereas binazine was not mutagenic in these strains. Both drugs were negative in mice micronucleus test.
[Mh] Termos MeSH primário: Anti-Hipertensivos/toxicidade
Hidralazina/toxicidade
Mutagênicos/toxicidade
Todralazina/toxicidade
[Mh] Termos MeSH secundário: Animais
Masculino
Camundongos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antihypertensive Agents); 0 (Mutagens); 26NAK24LS8 (Hydralazine); WEN3K83YKD (Todralazine)
[Em] Mês de entrada:9701
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:950101
[St] Status:MEDLINE



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