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[PMID]: 8928090 [Au] Autor: De La Cruz JP; Moreno A; Mérida F; García Campos J; Sánchez de la Cuesta F [Ad] Endereço: Department of Pharmacology and Therapeutics, School of Medicine, University of Malaga, Spain. [Ti] Título: The pyrimido-pyrimidine derivatives, dipyridamole, mopidamol and RA-642, prevent from retinal vascular defects in experimental diabetes mellitus. [So] Source: Thromb Res;81(3):327-37, 1996 Feb 01. [Is] ISSN: 0049-3848 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: We compared the effects of dipyridamole, RA-642, and mopidamol on platelet activity and thromboxane/prostacyclin balance in relation to the degree of retinal vascularization in a model of experimental streptozotocin-induced diabetes in rats. After 3 months, collagen-induced platelet aggregation in whole blood was 25% higher in diabetic animals than in nondiabetics. Dipyridamole inhibited 43% platelet aggregation, mopidamol 39%, and RA-642 36%. Platelet production of thromboxane B2 was 87% higher in untreated diabetic rats. Mopidamol and RA-642 produced a 46% and 41% inhibition of thromboxane B2. Dipyridamole did not inhibited thromboxane B2 synthesis. Aortic production of 6-keto-PGF1 alpha was 43% lower in untreated diabetic animals and showed no change after treatment with either mopidamol or RA-642. In contrast, dipyridamole caused a 90% increase in aortic production of prostacyclin. Computerized analysis of retinal vascularization showed that untreated diabetic rats had a 81% decrease in the area occupied by peroxidase-labelled vessels as compared with nondiabetics. Treatment with dipyridamole, mopidamol, and RA-642 caused 2.5-fold, 2.8-fold and four-fold increases, respectively, in the percentage of retinal surface occupied by peroxidase-labelled vessels. Differences in retinal vascularization between diabetic animals given RA-642 and nondiabetic controls were negligible. [Mh] Termos MeSH primário: Diabetes Mellitus Experimental/tratamento farmacológico Retinopatia Diabética/prevenção & controle Dipiridamol/farmacologia Mopidamol/farmacologia Inibidores da Agregação de Plaquetas/farmacologia Pirimidinas/farmacologia [Mh] Termos MeSH secundário: Animais Glicemia/metabolismo Diabetes Mellitus Experimental/complicações Diabetes Mellitus Experimental/metabolismo Retinopatia Diabética/metabolismo Epoprostenol/metabolismo Masculino Neovascularização Patológica/prevenção & controle Ratos Ratos Wistar Tromboxanos/metabolismo [Pt] Tipo de publicação: COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T [Nm] Nome de substância: 0 (Blood Glucose); 0 (Platelet Aggregation Inhibitors); 0 (Pyrimidines); 0 (Thromboxanes); 4Q0IWP8B8O (Mopidamol); 54093-30-0 (RA 642); 64ALC7F90C (Dipyridamole); DCR9Z582X0 (Epoprostenol) [Em] Mês de entrada: 9610 [Cu] Atualização por classe: 131121 [Lr] Data última revisão: 131121 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 960201 [St] Status: MEDLINE

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[PMID]: 8863175 [Au] Autor: Ambrus JL; Stadler I; Kulaylat M; Koreshi A; Akhtar S [Ad] Endereço: Department of Internal Medicine, University of New York. [Ti] Título: Hemorrheologic effects of pyrimido-pyrimidine derivatives. [So] Source: J Med;27(1-2):21-32, 1996. [Is] ISSN: 0025-7850 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: A series of pyrimido-pyrimidine derivatives were tested for their effect on membrane fluidity-deformability of human red blood cells and on human platelet aggregation. These agents were also tested for their intracellular cAMP increasing activity and proliferation inhibitory activity in neoplastic cells. The order of activity was established and clinical implications discussed. Several derivatives are under study as antineoplastic agents. [Mh] Termos MeSH primário: Hemorreologia Pirimidinas/farmacologia [Mh] Termos MeSH secundário: 3',5'-AMP Cíclico Fosfodiesterases/antagonistas & inibidores Difosfato de Adenosina/farmacologia Antineoplásicos/química Antineoplásicos/farmacologia Divisão Celular/efeitos dos fármacos AMP Cíclico/metabolismo Deformação Eritrocítica/efeitos dos fármacos Seres Humanos Melanoma/metabolismo Estrutura Molecular Mopidamol/farmacologia Agregação Plaquetária/efeitos dos fármacos Inibidores da Agregação de Plaquetas/química Inibidores da Agregação de Plaquetas/farmacologia Células Tumorais Cultivadas [Pt] Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T [Nm] Nome de substância: 0 (Antineoplastic Agents); 0 (Platelet Aggregation Inhibitors); 0 (Pyrimidines); 4Q0IWP8B8O (Mopidamol); 61D2G4IYVH (Adenosine Diphosphate); E0399OZS9N (Cyclic AMP); EC 3.1.4.17 (3',5'-Cyclic-AMP Phosphodiesterases) [Em] Mês de entrada: 9612 [Cu] Atualização por classe: 131121 [Lr] Data última revisão: 131121 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 960101 [St] Status: MEDLINE

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[PMID]: 8842690 [Au] Autor: De la Cruz JP; Olveira C; Gonzalez-Correa JA; Benítez A; Sánchez de la Cuesta F [Ad] Endereço: Department of Pharmacology and Therapeutics, School of Medicine, University of Málaga, Spain. [Ti] Título: Inhibition of ferrous-induced lipid peroxidation by dipyridamole, RA-642 and mopidamol in human lung tissue. [So] Source: Gen Pharmacol;27(5):855-9, 1996 Jul. [Is] ISSN: 0306-3623 [Cp] País de publicação: England [La] Idioma: eng [Ab] Resumo: 1. The in vitro production of ferrous-induced lipid peroxidation was 5.71 times higher in rat lung tissue than in human lung membranes. 2. The pyrimido-pyrimidine derivative RA-642 shows a more potent inhibition of ferrous-induced lipid peroxidation than dipyridamole; mopidamol had no effect. All the compounds showed higher anti-peroxidative effect in rat than in human lung tissue. [Mh] Termos MeSH primário: Antioxidantes/farmacologia Dipiridamol/farmacologia Compostos Ferrosos/antagonistas & inibidores Peroxidação de Lipídeos/efeitos dos fármacos Pulmão/metabolismo Mopidamol/farmacologia Pirimidinas/farmacologia [Mh] Termos MeSH secundário: Adulto Idoso Animais Feminino Compostos Ferrosos/farmacologia Seres Humanos Técnicas In Vitro Pulmão/efeitos dos fármacos Masculino Malondialdeído/metabolismo Meia-Idade Ratos Ratos Wistar Substâncias Reativas com Ácido Tiobarbitúrico/metabolismo Vitamina E/farmacologia [Pt] Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T [Nm] Nome de substância: 0 (Antioxidants); 0 (Ferrous Compounds); 0 (Pyrimidines); 0 (Thiobarbituric Acid Reactive Substances); 1406-18-4 (Vitamin E); 4Q0IWP8B8O (Mopidamol); 4Y8F71G49Q (Malondialdehyde); 54093-30-0 (RA 642); 64ALC7F90C (Dipyridamole) [Em] Mês de entrada: 9701 [Cu] Atualização por classe: 141120 [Lr] Data última revisão: 141120 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 960701 [St] Status: MEDLINE

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[PMID]: 7771466 [Au] Autor: Meehan KR; Zacharski LR; Moritz TE; Rickles FR [Ad] Endereço: Department of Veterans Affairs Medical & Regional Office Center, White River Junction, Vermont 05009-0001, USA. [Ti] Título: Pretreatment fibrinogen levels are associated with response to chemotherapy in patients with small cell carcinoma of the lung: Department of Veterans Affairs Cooperative Study 188. [So] Source: Am J Hematol;49(2):143-8, 1995 Jun. [Is] ISSN: 0361-8609 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: Small cell carcinoma of the lung (SCCL) responds commonly to combination chemotherapy but resistance to therapy follows. Prior reports have suggested that a relationship may exist between plasma fibrinogen levels and response to therapy in SCCL. This study was designed to determine the possible predictive value of the fibrinogen level for tumor response (chemoresistance) in SCCL. Pretreatment fibrinogen levels were correlated with outcome and response to therapy in a cohort of 119 previously untreated patients with SCCL who were admitted to VA Cooperative Study 188. Higher pretreatment fibrinogen levels at diagnosis correlated significantly with more advanced stage of disease at entry (P < 0.001) and with reduced overall survival (P = 0.030). In addition, higher pretreatment fibrinogen levels were correlated significantly with a reduced likelihood of achieving subsequent disease regression with combination chemotherapy (P = 0.005). Because several clinical trials have shown that anticoagulant therapy improves tumor response rates and survival of SCCL, we postulate that tumor cell thrombin generation not only promotes SCCL growth but may also be primarily responsible for both increased fibrinogen levels and for resistance to chemotherapy. These findings provide incentive for studies of thrombin effects on the development of multidrug resistance, and for new clinical trials of more potent and specific inhibitors of thrombin that may further improve tumor response and survival in SCCL. [Mh] Termos MeSH primário: Carcinoma de Células Pequenas/sangue Fibrinogênio/análise Neoplasias Pulmonares/sangue [Mh] Termos MeSH secundário: Carcinoma de Células Pequenas/tratamento farmacológico Carcinoma de Células Pequenas/fisiopatologia Estudos de Coortes Resistência a Medicamentos Fibrinolisina/análise Fibrinopeptídeo A/análise Fibrinopeptídeo B/análise Seres Humanos Neoplasias Pulmonares/tratamento farmacológico Neoplasias Pulmonares/fisiopatologia Mopidamol/uso terapêutico Ensaios Clínicos Controlados Aleatórios como Assunto Análise de Regressão Trombina/análise [Pt] Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.; RESEARCH SUPPORT, U.S. GOV'T, P.H.S. [Nm] Nome de substância: 25422-31-5 (Fibrinopeptide A); 36204-23-6 (Fibrinopeptide B); 4Q0IWP8B8O (Mopidamol); 9001-32-5 (Fibrinogen); EC 3.4.21.5 (Thrombin); EC 3.4.21.7 (Fibrinolysin) [Em] Mês de entrada: 9507 [Cu] Atualização por classe: 131121 [Lr] Data última revisão: 131121 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 950601 [St] Status: MEDLINE

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[PMID]: 7701482 [Au] Autor: De La Cruz JP; Villalobos MA; Palacios R; Smith-Agreda JM; Sánchez de la Cuesta F [Ad] Endereço: Department of Pharmacology and Therapeutics, School of Medicine, University of Málaga, Spain. [Ti] Título: In vitro effect of mopidamol on platelet-subendothelium interaction. [So] Source: Thromb Res;77(1):97-103, 1995 Jan 01. [Is] ISSN: 0049-3848 [Cp] País de publicação: United States [La] Idioma: eng [Mh] Termos MeSH primário: Endotélio Vascular/efeitos dos fármacos Mopidamol/farmacologia Inibidores da Agregação de Plaquetas/farmacologia Agregação Plaquetária/efeitos dos fármacos [Mh] Termos MeSH secundário: Adulto Comunicação Celular/efeitos dos fármacos Dipiridamol/farmacologia Seres Humanos Técnicas In Vitro Masculino Perfusão [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Platelet Aggregation Inhibitors); 4Q0IWP8B8O (Mopidamol); 64ALC7F90C (Dipyridamole) [Em] Mês de entrada: 9505 [Cu] Atualização por classe: 141120 [Lr] Data última revisão: 141120 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 950101 [St] Status: MEDLINE

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[PMID]: 8304965 [Au] Autor: De La Cruz JP; Ortega G; Sánchez de la Cuesta F [Ad] Endereço: Department of Pharmacology and Therapeutics, School of Medicine, University of Málaga, Spain. [Ti] Título: Differential effects of the pyrimido-pyrimidine derivatives, dipyridamole and mopidamol, on platelet and vascular cyclooxygenase activity. [So] Source: Biochem Pharmacol;47(2):209-15, 1994 Jan 20. [Is] ISSN: 0006-2952 [Cp] País de publicação: England [La] Idioma: eng [Ab] Resumo: The chronic administration of 10 mg/kg/day of dipyridamole to rats produced 33.7% inhibition of platelet aggregation induced with ADP and a 93% increase in 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) in vascular samples, versus saline-treated rats. Mopidamol, 8.3 mg/kg/day, caused 50.6% inhibition of ADP-induced platelet aggregation, 37.6% inhibition of aggregation induced with arachidonic acid, a 47.6% decrease in serum levels of thromboxane B2 and a 23.7% increase in the vascular production of 6-keto-PGF1 alpha, versus saline-treated rats. Dipyridamole showed a higher in vitro anti-aggregating effect in whole blood (IC50 6.6 microM) than in platelet-rich plasma (PRP) (IC50 210 microM), when ADP was used as inducer, and had no effect in the presence of arachidonic acid. Mopidamol exerted a similar effect in whole blood (IC50 3.7-20 microM, depending on the inducer) and PRP (IC50 11-17.3 microM), and showed a dose-dependent inhibition of platelet aggregation and thromboxane B2 synthesis induced with arachidonic acid (IC50 16.8-22.3 microM). Mopidamol also inhibited enzymatically induced lipid peroxidation) (IC50 89 +/- 5.9 mumol/L) and had no effect on free radical-induced lipid peroxidation. The dose-dependent increase in 6-keto-PGF1 alpha in vascular samples after incubation with dipyridamole showed a negative linear correlation with inhibition of lipid peroxidation (r2 = 0.77). It is concluded that the phosphodiesterase inhibitors, dipyridamole and mopidamol, interfere in a different manner with platelet function. It seems that mopidamol may also exert a selective effect on platelet thromboxane synthesis. [Mh] Termos MeSH primário: Plaquetas/enzimologia Vasos Sanguíneos/enzimologia Dipiridamol/farmacologia Mopidamol/farmacologia Prostaglandina-Endoperóxido Sintases/metabolismo [Mh] Termos MeSH secundário: Animais Inibidores de Ciclo-Oxigenase/farmacologia Ativação Enzimática/efeitos dos fármacos Epoprostenol/biossíntese Seres Humanos Peroxidação de Lipídeos/efeitos dos fármacos Masculino Agregação Plaquetária/efeitos dos fármacos Ratos Ratos Wistar Tromboxano A2/biossíntese [Pt] Tipo de publicação: COMPARATIVE STUDY; JOURNAL ARTICLE [Nm] Nome de substância: 0 (Cyclooxygenase Inhibitors); 4Q0IWP8B8O (Mopidamol); 57576-52-0 (Thromboxane A2); 64ALC7F90C (Dipyridamole); DCR9Z582X0 (Epoprostenol); EC 1.14.99.1 (Prostaglandin-Endoperoxide Synthases) [Em] Mês de entrada: 9403 [Cu] Atualização por classe: 131121 [Lr] Data última revisão: 131121 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 940120 [St] Status: MEDLINE

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[PMID]: 8287616 [Au] Autor: Schirner M; Lichtner RB; Schneider MR [Ad] Endereço: Research Laboratories of Schering AG, Berlin, Germany. [Ti] Título: The stable prostacyclin analogue Cicaprost inhibits metastasis to lungs and lymph nodes in the 13762NF MTLn3 rat mammary carcinoma. [So] Source: Clin Exp Metastasis;12(1):24-30, 1994 Jan. [Is] ISSN: 0262-0898 [Cp] País de publicação: Netherlands [La] Idioma: eng [Ab] Resumo: Prostacyclin and its stable analogues have been shown to interfere specifically with certain steps of the metastatic cascade. The antimetastatic activity of the stable prostacyclin analogue Cicaprost (Schering AG) on haematogenous metastasis in a series of tumours in rats and mice has been well established. In order to test the effect of Cicaprost on lymphogenous metastasis we chose the metastatic cell clone MTLn3 derived from the 13762NF rat mammary carcinoma. The effect of Cicaprost on prevention of lung metastasis, lymph node metastasis and primary tumour growth was investigated. Cicaprost given in daily doses of 0.01, 0.03 and 0.1 mg/kg orally, reduced the number of lung metastases in a dose-dependent manner. Whereas the median number of lung metastases in the controls was greater than 1000, Cicaprost at a dose of 0.1 mg/kg reduced the number of lung metastases to between 11 and 100. The weight of the ipsilateral axillary lymph nodes was diminished by Cicaprost to 30-50% of controls. Moreover, metastasis to the contralateral axillary lymph node was completely inhibited by Cicaprost at all three doses tested. Cicaprost did not influence the growth rate of the MTLn3 cell clone implanted into the mammary fat pad or the weight of the primary tumour at the end of treatment. In conclusion, in addition to its dose-dependent effect on haematogenous metastasis, Cicaprost strongly inhibits lymph node metastasis. [Mh] Termos MeSH primário: Antineoplásicos/uso terapêutico Epoprostenol/análogos & derivados Neoplasias Pulmonares/secundário Metástase Linfática/prevenção & controle Neoplasias Mamárias Experimentais/tratamento farmacológico [Mh] Termos MeSH secundário: Animais Relação Dose-Resposta a Droga Epoprostenol/uso terapêutico Feminino Neoplasias Pulmonares/prevenção & controle Neoplasias Mamárias Experimentais/patologia Mopidamol/uso terapêutico Ratos Ratos Endogâmicos F344 [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Antineoplastic Agents); 4Q0IWP8B8O (Mopidamol); DCR9Z582X0 (Epoprostenol); NE94J8CAMD (cicaprost) [Em] Mês de entrada: 9402 [Cu] Atualização por classe: 170822 [Lr] Data última revisão: 170822 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 940101 [St] Status: MEDLINE

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[PMID]: 7870694 [Au] Autor: de la Cruz JP; Moreno A; Mérida F; García-Campos J; Sánchez de la Cuesta F [Ad] Endereço: Department of Pharmacology and Therapeutics, School of Medicine, University of Málaga, Spain. [Ti] Título: The pyrimido-pyrimidine derivatives, dipyridamole and RA-642, reduce opacification of crystalline lens in diabetic rats. [So] Source: Pharmacol Toxicol;75(5):250-4, 1994 Nov. [Is] ISSN: 0901-9928 [Cp] País de publicação: Denmark [La] Idioma: eng [Ab] Resumo: We assessed the effect of dipyridamole, RA-642 and mopidamol, on lenticular opacities in a model of experimental diabetic cataracts in rats. All three pyrimido-pyrimidine derivatives caused a statistically significant reduction of opacification in crystalline lens as compared with untreated diabetic animals. The production of superoxide anions (phenazine methosulphate [PMS]-induced nitroblue tetrazolium [NBT] reduction) showed a decrease of 81.6%, 78.9% and 1.8% in lens tissue homogenates from rats treated with dipyridamole, RA-642 and mopidamol, respectively. Dipyridamole and RA-642 produced a statistically significant inhibition (50% and 64.8%, respectively) of lipid peroxidation (ferrous sulphate and ascorbic acid [FeAs]-induced malondialdehyde [MDA] production) as compared with the group of untreated diabetic rats. Mopidamol did not exert any inhibitory effect on lipid peroxidation. There was a statistically significant correlation between opacification of lens and PMS-induced NBT reduction and FeAs-induced MDA production. We conclude that the protective effect of dipyridamole and RA-642 from free radical damage to crystalline lens in the model of experimental diabetes used in this study, is the result of the antioxidant action of these compounds. The effect exerted by mopidamol, however, suggest a possible complementary effect of the pyrimido-pyrimidine derivatives through interaction with other mechanisms (e.g., the sorbitol pathway) implicated in the development of cataracts. [Mh] Termos MeSH primário: Cardiotônicos/farmacologia Catarata/prevenção & controle Diabetes Mellitus Experimental/complicações Dipiridamol/farmacologia Cristalino/efeitos dos fármacos Pirimidinas/farmacologia [Mh] Termos MeSH secundário: Animais Glicemia/análise Catarata/etiologia Catarata/patologia Cristalino/metabolismo Cristalino/patologia Peroxidação de Lipídeos/efeitos dos fármacos Masculino Malondialdeído/metabolismo Mopidamol/farmacologia Ratos Ratos Wistar Superóxidos/metabolismo [Pt] Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T [Nm] Nome de substância: 0 (Blood Glucose); 0 (Cardiotonic Agents); 0 (Pyrimidines); 11062-77-4 (Superoxides); 4Q0IWP8B8O (Mopidamol); 4Y8F71G49Q (Malondialdehyde); 54093-30-0 (RA 642); 64ALC7F90C (Dipyridamole) [Em] Mês de entrada: 9503 [Cu] Atualização por classe: 131121 [Lr] Data última revisão: 131121 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 941101 [St] Status: MEDLINE

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[PMID]: 8453569 [Au] Autor: Tzanakakis GN; Agarwal KC; Vezeridis MP [Ad] Endereço: Surgical Service Veterans Administration Medical Center, Providence, Rhode Island. [Ti] Título: Prevention of human pancreatic cancer cell-induced hepatic metastasis in nude mice by dipyridamole and its analog RA-233. [So] Source: Cancer;71(8):2466-71, 1993 Apr 15. [Is] ISSN: 0008-543X [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: BACKGROUND: Several studies have provided evidence suggesting that platelets play a key role in tumor metastasis. A number of antiplatelet agents have been used to prevent tumor metastasis in animal models and humans. Antiplatelet agents, dipyridamole (adenosine transport inhibitor), and RA-233 (inhibitor of cAMP PDE) were used to prevent tumor-cell-platelet interactions both in in vitro and in vivo systems; however, the data were not very conclusive. METHODS: Our studies used dipyridamole and RA-233 alone and in combination to investigate their effects on human pancreatic tumor cells (RWP-2)-induced platelet aggregation in human blood and on hepatic metastasis in nude mice. To examine effects of dipyridamole and RA-233 on liver metastasis, the tumor cells (RWP-2) were injected intrasplenically in nude mice grouped into control, dipyridamole (8 mg/kg), RA-233 (8 mg/kg), and dipyridamole plus RA-233 (8 mg/kg each). The agents were administered intraperitoneally 1 hour before and 24 hours after the tumor cell injection. RESULTS: When dipyridamole and RA-233 were used alone, only weak to moderate effects were seen on RWP-2 tumor cell-induced platelet aggregation. However, these agents, when combined, strongly inhibited the tumor cell-induced aggregation in human platelet-rich plasma. In tumor metastasis experiments, reductions of approximately 70% in hepatic nodules and 90% in surface area occupied by the tumor were seen with the combination treatment (dipyridamole plus RA-233) as compared with the control group of mice. CONCLUSIONS: This study suggests that the combination of dipyridamole and RA-233 provides an effective intervention for the antithrombotic approach to the treatment of cancer metastases. [Mh] Termos MeSH primário: Dipiridamol/farmacologia Neoplasias Hepáticas/prevenção & controle Neoplasias Hepáticas/secundário Mopidamol/farmacologia Neoplasias Pancreáticas Agregação Plaquetária/efeitos dos fármacos [Mh] Termos MeSH secundário: Adenosina/sangue Animais Ensaios de Seleção de Medicamentos Antitumorais Sinergismo Farmacológico Seres Humanos Neoplasias Hepáticas/sangue Camundongos Camundongos Nus Neoplasias Pancreáticas/sangue Células Tumorais Cultivadas [Pt] Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.; RESEARCH SUPPORT, U.S. GOV'T, P.H.S. [Nm] Nome de substância: 4Q0IWP8B8O (Mopidamol); 64ALC7F90C (Dipyridamole); K72T3FS567 (Adenosine) [Em] Mês de entrada: 9304 [Cu] Atualização por classe: 131121 [Lr] Data última revisão: 131121 [Sb] Subgrupo de revista: AIM; IM [Da] Data de entrada para processamento: 930415 [St] Status: MEDLINE

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[PMID]: 1522764 [Au] Autor: de la Cruz JP; Carrasco T; Ortega G; Sanchez de la Cuesta F [Ad] Endereço: Department of Pharmacology and Therapeutics, School of Medicine, University of Málaga, Spain. [Ti] Título: Inhibition of ferrous-induced lipid peroxidation by pyrimido-pyrimidine derivatives in human liver membranes. [So] Source: Lipids;27(3):192-4, 1992 Mar. [Is] ISSN: 0024-4201 [Cp] País de publicação: Germany [La] Idioma: eng [Ab] Resumo: The effects of pyrimido-pyrimidine derivatives (dipyridamole, RA-642, and RA-233) on lipid peroxidation, using d-alpha-tocopherol as standard, were studied in enriched membrane fractions from human and rat hepatocytes. Equimolar concentrations of ferrous sulfate and ascorbic acid were used to induce lipid peroxidation. The amount of peroxidized lipids observed in membrane fractions from human liver was smaller than in those from rat liver. In both species, however, pyrimido-pyrimidine derivatives, except for RA-233 in rat liver, inhibited lipid peroxidation dose-dependently in the following sequence: RA-642 greater than dipyridamole greater than d-alpha-tocopherol RA-233. [Mh] Termos MeSH primário: Membrana Celular/metabolismo Compostos Ferrosos/farmacologia Peroxidação de Lipídeos/efeitos dos fármacos Fígado/metabolismo Mopidamol/farmacologia Pirimidinas/farmacologia [Mh] Termos MeSH secundário: Animais Ácido Ascórbico/farmacologia Cardiotônicos/farmacologia Membrana Celular/efeitos dos fármacos Dipiridamol/farmacologia Seres Humanos Cinética Malondialdeído/metabolismo Ratos Especificidade da Espécie Vitamina E/farmacologia [Pt] Tipo de publicação: COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T [Nm] Nome de substância: 0 (Cardiotonic Agents); 0 (Ferrous Compounds); 0 (Pyrimidines); 1406-18-4 (Vitamin E); 39R4TAN1VT (ferrous sulfate); 4Q0IWP8B8O (Mopidamol); 4Y8F71G49Q (Malondialdehyde); 54093-30-0 (RA 642); 64ALC7F90C (Dipyridamole); PQ6CK8PD0R (Ascorbic Acid) [Em] Mês de entrada: 9210 [Cu] Atualização por classe: 170905 [Lr] Data última revisão: 170905 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 920301 [St] Status: MEDLINE

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1			PalavrasDescritor de assuntoDescritor de assunto primárioLimitesAutorPalavras do títuloPalavras do resumoIdiomaPaís de publicaçãoNome de substânciaNome de pessoa como assuntoRevistaAssunto de RevistaISSNTipo de publicaçãoIdentificador únicoMês de entradaAno de publicaçãoTexto completoAtualização por classeCategoria DeCSCategoria DeCS explodidaCategoria CID-10SubSetsPais de AfiliaçãoAfiliaçãoAfiliação 2
2	and or and not		PalavrasDescritor de assuntoDescritor de assunto primárioLimitesAutorPalavras do títuloPalavras do resumoIdiomaPaís de publicaçãoNome de substânciaNome de pessoa como assuntoRevistaAssunto de RevistaISSNTipo de publicaçãoIdentificador únicoMês de entradaAno de publicaçãoTexto completoAtualização por classeCategoria DeCSCategoria DeCS explodidaCategoria CID-10SubSetsPais de AfiliaçãoAfiliaçãoAfiliação 2
3	and or and not		PalavrasDescritor de assuntoDescritor de assunto primárioLimitesAutorPalavras do títuloPalavras do resumoIdiomaPaís de publicaçãoNome de substânciaNome de pessoa como assuntoRevistaAssunto de RevistaISSNTipo de publicaçãoIdentificador únicoMês de entradaAno de publicaçãoTexto completoAtualização por classeCategoria DeCSCategoria DeCS explodidaCategoria CID-10SubSetsPais de AfiliaçãoAfiliaçãoAfiliação 2

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