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Academic literature on the topic 'Primaquin'

Author: Grafiati

Published: 4 June 2021

Last updated: 18 February 2022

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Journal articles on the topic "Primaquin"

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Hang, Zhang Zhong. "Elimination of the gametocytes of Theileria annulata of cattle by primaquin phosphate." Veterinary Parasitology 23, no. 1-2 (1987): 11–21. http://dx.doi.org/10.1016/0304-4017(87)90021-5.

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Vinnemeier, Christof, and Thierry Rolling. "Prophylaxe und Therapie der Malaria: aktuelle Empfehlungen." DMW - Deutsche Medizinische Wochenschrift 143, no. 07 (2018): 472–75. http://dx.doi.org/10.1055/s-0044-100818.

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Was ist neu? Epidemiologie Weltweit sind die Malaria-Inzidenzen rückläufig. Die Zahl der nach Deutschland importierten Fälle blieb zuletzt auf hohem Niveau stabil. Von größter Bedeutung ist es gut bekannte Risikogruppen mit Beratungsangeboten zu erreichen, z. B. Reisende auf Verwandtenbesuch in Endemiegebieten. Prophylaxe Mefloquin steht seit 2013 in Deutschland nur noch als Einzelimport zur Verfügung, bleibt jedoch für bestimmte Personengruppen weiter ein wichtiges Prophylaktikum. Die notfallmäßige Selbsttherapie der Malaria, die gängige Praxis für Reisende in Länder mit niedrigem und mittlerem Übertragungsrisiko ist, wird in der Reisemedizin zunehmend kritisiert und sollte zielgerichteter eingesetzt werden. Therapie der Malaria tropica Patienten mit einem höheren Körpergewicht müssen nach einer Therapie engmaschig nachbeobachtet werden, da sie ein höheres Risiko einer Rekrudeszenz haben. Artesunat ist Mittel der Wahl zur Therapie der komplizierten Malaria tropica. Auch hier ist eine konsequente Kontrolle nach Therapieende notwendig, um eine mit Artesunat assoziierte hämolytische Anämie frühzeitig zu erfassen. Malaria tertiana Seit 2014 gab es in Deutschland eine Zunahme von Patienten mit einer Malaria tertiana, insbesondere bei Migranten aus Eritrea. Aufgrund der unzureichenden Gesundheitsversorgung der Flüchtenden haben nicht alle Patienten die bei Plasmodium vivax notwendige Rezidivprophylaxe mit Primaquin erhalten.

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Octabiano G, Reinaldi, I. Nyoman Yesaya C, Zega Agustian, et al. "Mixed Infection of Vivax and Falciparum Malaria with Severe Manifestations of Malaria at the General Hospital of the Christian University of Indonesia: A Case Report." Journal of Asian Multicultural Research for Medical and Health Science Study 2, no. 2 (2021): 28–32. http://dx.doi.org/10.47616/jamrmhss.v2i2.96.

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Malaria is still a health problem in Indonesia. The number of malaria cases according to the 2018 RISKESDAS reached 8076 cases, and the highest number was obtained from Papua province with 3,334 cases. Multiple infection malaria in Indonesia according to RISKESDAS 2018, has a rate of 0.01% of the total cases, namely Plasmodium Falciparum malaria and Plasmodium non Falciparum malaria. A 47 year old man was referred from the clinic with complaints of high fever preceded by chills 10 days before being admitted to the hospital. Accompanied by shortness of breath, unable to get off the treatment bed due to feeling very weak, nauseous, sick and having a bulging stomach. Physical examination revealed a pale conjunctiva, ronkhi in the lower field of the right lung, dim percussion in the basal of the left lung, hepatomegaly, splenomegaly, shifting dullness. ring form vivax, on chest X-ray found a left pleural effusion. It is known that the patient previously lived in Papua from September 2018 to May 2019. During treatment, the patient was given artesunate injection therapy, dihydroartemisin + piperaquine and primaquin for seven days of treatment. At the end of the treatment, another chest X-ray was performed and re-examination of the peripheral blood smear, no more pleural effusions were found and no parasites were found on re-examination of the peripheral blood smear. Mixed infection of vivax and falciparum malaria, is a rare case that may occur in endemic areas where both plasmodium can be found. The prevalence in Indonesia according to RISKESDAS is only about 0.01% of all malaria cases in Indonesia.

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Pareek, Anil, Nitin Chandurkar, Nithya Gogtay, et al. "Sustained Release Formulation of Primaquine for Prevention of Relapse of Plasmodium vivax Malaria: A Randomized, Double-Blind, Comparative, Multicentric Study." Malaria Research and Treatment 2015 (August 20, 2015): 1–8. http://dx.doi.org/10.1155/2015/579864.

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Background. Primaquine is used to eradicate latent Plasmodium vivax parasite from liver, with administration of standard dose daily up to 14 days. We studied efficacy, safety, and tolerability of sustained release (SR) formulation of primaquine in comparison with conventional primaquine in preventing relapse of P. vivax malaria. Methods. Microscopically confirmed cases of P. vivax malaria received chloroquine therapy for three days. Aparasitemic and asymptomatic patients were then randomized to receive either conventional primaquine 15 mg for 14 days or primaquine SR 15 mg for 14 days, or primaquine SR 30 mg for seven days. Results. Of the 360 patients, who received chloroquine therapy, 358 patients were randomized. Two-hundred eighty-eight patients completed six-month follow-up and four patients (three: conventional primaquine 15 mg (2.86%), one: primaquine SR 30 mg (0.93%)) showed relapse confirmed by PCR genotyping. Drug compliance was significantly better in primaquine SR 30 mg group (95.57%, p=0.039) without any serious adverse events. Conclusion. Primaquine SR 15 mg and primaquine SR 30 mg could be an effective alternative to conventional primaquine 15 mg due to their comparable cure rates and safety profile. Shorter treatment duration with primaquine SR 30 mg may increase patient compliance and may further reduce relapse rates. Clinical Trial Registration. This trial is registered with CTRI/2010/091/000245.

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Sutanto, Inge, Bagus Tjahjono, Hasan Basri, et al. "Randomized, Open-Label Trial of Primaquine against Vivax Malaria Relapse in Indonesia." Antimicrobial Agents and Chemotherapy 57, no. 3 (2012): 1128–35. http://dx.doi.org/10.1128/aac.01879-12.

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ABSTRACTRadical cure ofPlasmodium vivaxinfection applies blood schizontocidal therapy against the acute attack and hypnozoitocidal therapy against later relapse. Chloroquine and primaquine have been used for 60 years in this manner. Resistance to chloroquine by the parasite now requires partnering other blood schizontocides with primaquine. However, the safety and efficacy of primaquine against relapse when combined with other drugs have not been demonstrated. This randomized, open-label, and relapse-controlled trial estimated the efficacy of primaquine against relapse when administered with quinine or dihydroartemisinin-piperaquine for treatment of the acute infection. Among 650 soldiers who had returned to their malaria-free base in Java, Indonesia, after 12 months in malarious Papua, Indonesia, 143 with acuteP. vivaxmalaria were eligible for study. One hundred sixteen enrolled subjects were randomized to these treatments: artesunate (200-mg dose followed by 100 mg/day for 6 days), quinine (1.8 g/day for 7 days) plus concurrent primaquine (30 mg/day for 14 days), or dihydroartemisinin (120 mg) plus piperaquine (960 mg) daily for 3 days followed 25 days later by primaquine (30 mg/day for 14 days). Follow-up was for 12 months. One hundred thirteen subjects were analyzable. Relapse occurred in 32 of 41 (78%) subjects administered artesunate alone (2.71 attacks/person-year), 7 of 36 (19%) administered quinine plus primaquine (0.23 attack/person-year), and 2 of 36 (6%) administered dihydroartemisinin-piperaquine plus primaquine (0.06 attack/person-year). The efficacy of primaquine against relapse was 92% (95% confidence interval [CI] = 81% to 96%) for quinine plus primaquine and 98% (95% CI = 91% to 99%) for dihydroartemisinin-piperaquine plus primaquine. Antirelapse therapy with primaquine begun a month after treatment of the acute attack with dihydroartemisinin-piperaquine proved safe and highly efficacious against relapse byP. vivaxacquired in Papua, Indonesia.

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&NA;. "Primaquine." Reactions Weekly &NA;, no. 1324 (2010): 29–30. http://dx.doi.org/10.2165/00128415-201013240-00089.

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&NA;. "Primaquine." Reactions Weekly &NA;, no. 428 (1992): 11. http://dx.doi.org/10.2165/00128415-199204280-00056.

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&NA;. "Primaquine." Reactions Weekly &NA;, no. 1095 (2006): 23. http://dx.doi.org/10.2165/00128415-200610950-00079.

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&NA;. "Primaquine." Reactions Weekly &NA;, no. 314 (1990): 10. http://dx.doi.org/10.2165/00128415-199003140-00055.

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&NA;. "Primaquine." Reactions Weekly &NA;, no. 731 (1998): 10. http://dx.doi.org/10.2165/00128415-199807310-00034.

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Dissertations / Theses on the topic "Primaquin"

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Giampieri, Giovanna [Verfasser], and Ioannis [Akademischer Betreuer] Mylonas. "Untersuchungen zur antitumoralen Wirkung von Malariamedikamenten auf Brustkrebszellen am Beispiel von Primaquin und Chloroquin / Giovanna Giampieri ; Betreuer: Ioannis Mylonas." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2018. http://d-nb.info/1163534218/34.

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Barros, Rita de Cássia Mendes de. "Mecanismo de oxidação eletroquímica e determinação analítica de primaquina - algumas aplicações de eletrodos de diamante dopado com boro." Universidade de São Paulo, 2007. http://www.teses.usp.br/teses/disponiveis/46/46133/tde-29112007-161126/.

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A primaquina (PQ), um derivado 8-aminoquinolínico [8-(4-amino-1-metilbutilamino)-6metoxiquinolina], é um fármaco normalmente usado contra a malária, mas tem sido, também empregado no tratamento da doença de Chagas, agindo, muito eficazmente, como agente tripanomicida, por intermédio de seus metabólitos. O metabólito 5hidroxiprimaquina (5-HPQ), formado pela oxidação da primaquina dentro do organismo humano, foi identificado em fluídos biológicos e é considerado o principal produto com ação citotóxica sobre o Trypanosoma cruzi. Técnicas eletroquímicas foram empregadas para estudar o mecanismo de oxidação da PQ in vitro na tentativa de correlacionar os resultados obtidos, com os dados disponíveis de estudos in vivo. Utilizou-se eletrodo de carbono vítreo (ECV) e diferentes tipos de técnicas, como voltametria cíclica, voltametria de pulso diferencial e cronoamperometria, trabalhando-se em meio aquoso, tampão Britton-Robson, pH 7,40, para determinação do número de elétrons envolvidos na etapa determinante da reação. O mecanismo eletroquímico de oxidação da PQ, envolveu a perda de 1 elétron em um processo irreversível, registrado em Epa,1 a +0,788 V, resultando na formação de cátion radical durante a primeira varredura no sentido positivo de potencial. Após a inversão da varredura de potencial, registrou-se um pico catódico, Epc,1 a -0,160 V, dependente do processo principal. Voltamogramas cíclicos realizados em meio não aquoso indicaram que a etapa eletroquímica inicial é seguida de uma etapa química envolvendo a captura nucleofílica do cátion radical. No segundo ciclo de varredura, registrou-se um segundo pico anódico, Epa,2, a -0,079 V, componente anódico de Epc,1. Assim, um novo par redox passou a ser observado, dependente da oxidação primária da PQ, mas registrado em potencial muito menos positivo do que a oxidação da PQ, composto de partida. Este novo processo redox, típico do par quinonalhidroquinona, está envolvido em vários outros processos descritos na literatura, e pressupõe que, após a captura nucleofílica do cátion radical, ocorra outra etapa eletroquímica, no potencial aplicado, envolvendo a perda de 3 elétrons e 3 prótons, com formação de uma quinona-i mina. A subseqüente hidrólise da imina produz o derivado quinoidal e diamina primária. Voltamogramas cíclicos registrados em solução de 5-HPQ e m-anisidina confirmaram o mecanismo proposto. Devido à ausência de fenõmenos de adsorção, utilizou-se com sucesso o eletrodo de diamante dopado com boro (EDDB), no formato pIano, para a determinação analítica de PQ em formulação farmacêutica comercial, empregando-se a voltametria de pulso diferencial. Enquanto o ECV foi mais efetivo para a proposição do mecanismo, principalmente devido às características de adsorção superficial, o EDDB permitiu o desenvolvimento de um método analítico para a quantificação de PQ, devido à ausência de adsorção superficial.<br>Primaquine (PQ), an 8-aminoquinolinic compound, is the clinical drug of choice for the radical cure of relapsing malaria. This drug has also been being used against the Chagas disease, acting very efficiently, through their metabolites, which present trypanosomicide action. The metabolite 5-hydroxyprimaquine (5-HPQ) was identified in human biological fluids, during in vivo studies, as the main oxidation product of PQ, with cytotoxic action against Trypanosoma cruzi. Electrochemical techniques were used to study, in vitro, the PQ oxidation redox mechanism and the goal was to try correlating the electrochemical data to the biological information, previously reported. Glassy carbon electrode (GCE) associated to cyclic and differential pulse voltammetry and cronoamperommetry in aqueous media, pH 7.40, were used to determine de number of electrons involved in the determinant step of PQ electrochemical oxidation. The primary oxidation of PQ involved the loss of 1 electron in an irreversible process recorded at Epa,1 = +0,788 V, to produce a cation radical, during the first anodic scan. Reverting the potential sweeping a cathodic peak, Epc,1, was recorded at -0,160 V, which was dependent of Epa,1. Cyclic voltammograms recorded in DMF showed that the initial electrochemical step is followed by a chemical reaction involving the nucleophilic capture of the cation radical. During the second scan, a new anodic peak (Epa,2) was recorded at -0,079 V and corresponds to the anodic component of Epc,1. Therefore a new redox couple, recorded at less positive potential than the PQ oxidation was always observed and shows similar characteristics to those observed for quinoneJhydroquinone redox couple, which is involved is several another electrochemical processes described in the literature. The process presupposes that the nucleophilic capture of the cation radical is followed by another electrochemical step involving the loss of 3 electrons and 3 protons to produce a quinone-imine structure. The further imine hydrolysis produces the quinoidal compound and primary diamine. The purposed mechanism was confirmed by the cyclic voltammograms recorded in 5-HPQ solutions as well as in the solutions of similar compound such as m-anisidine. PQ was determined in commercial pharmaceutical formulations by using differential pulse voltammetry at boron doped diamond electrode (BDDE) associated to the standard addition method. While the GCE was more effective for the mechanism proposition, mainly due its superficial adsorption characteristics, the BDDE, due low superficial adsorptive effects, permitted the development of analytical method for the PQ quantification.

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Zanucoli, Fábio dos Santos Machado 1990. "Desenvolvimento de estratégia terapêutica para neuroinflamação autoimune utilizando o antimalárico primaquina." [s.n.], 2015. http://repositorio.unicamp.br/jspui/handle/REPOSIP/316948.

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Orientador: Liana Maria Cardoso Verinaud<br>Dissertação (mestrado) - Universidade Estadual de Campinas, Instituto de Biologia<br>Made available in DSpace on 2018-08-27T08:18:08Z (GMT). No. of bitstreams: 1 Zanucoli_FabiodosSantosMachado_M.pdf: 3072241 bytes, checksum: 66a7959825671f33da79f21f4dbeda55 (MD5) Previous issue date: 2015<br>Resumo: A esclerose múltipla (EM) é uma doença inflamatória crônica de origem autoimune que afeta o sistema nervoso central (SNC), provocando disfunções neurológicas em decorrência de desmielinização axonal, principalmente na substância branca dos órgãos do SNC. A doença acomete mais de 2 milhões de pessoas no mundo todo e não tem cura. As abordagens terapêuticas utilizadas com sucesso consistem na aplicação de anticorpos monoclonais, citocinas imunomoduladoras e fármacos antiinflamatórios. Ainda assim, tais estratégias são dependentes de produtos de alto custo e toxicidade. A utilização de fármacos antimaláricos no tratamento da Encefalomielite Autoimune Experimental (EAE, modelo experimental de EM), como cloroquina e diidroartemisinina, tem apresentado resultados promissores na atenuação do quadro clínico dos camundongos; entretanto, os efeitos tóxicos dessas substâncias constituem um importante fator limitante para a utilização clínica. Neste sentido, o presente trabalho teve por objetivo caracterizar os efeitos terapêuticos da primaquina (PQ), um fármaco antimalárico análogo à cloroquina mas com toxicidade reduzida, na EAE emvcamundongos C57BL/6. Para tanto, camundongos foram tratados com PQ por via intraperitoneal (i.p.) por cinco dias consecutivos e os efeitos da administração direta foram avaliados sobre as subpopulações de linfócitos T esplênicos. Semelhantemente, camundongos portadores de EAE foram tratados com PQ como acima e o desenvolvimento da doença foi avaliado. Os resultados obtidos mostraram uma redução significativa na severidade da EAE em camundongos tratados com primaquina em comparação com animais pertencentes ao grupo controle. A melhora no quadro clínico se correlacionou com (i) aumento na expressão de genes de citocinas anti-inflamatórias e decréscimo na expressão de genes de citocinas inflamatórias, (ii) redução na ativação de micróglia e (iii) diminuição da reatividade glial no SNC de camundongos tratados com PQ em relação aos não tratados. Também se verificou um aumento na frequência de células T reguladoras em baços de camundongos tratados com PQ. Posteriormente, células T reguladoras (Treg, CD4+CD25+) e células T efetoras (CD4+CD25- ) foram isoladas de baços de camundongos tratados com PQ e transferidas adotivamente a camundongos portadores de EAE. Foi observada uma redução na severidade da EAE em camundongos recipientes de células Treg em comparação com camundongos recipientes de células T efetoras. De forma semelhante ao observado em camundongos tratados diretamente com PQ, a menor severidade da EAE se correlacionou com redução na expressão de mediadores inflamatórios e de reatividade glial no SNC. A capacidade imunossupressora de PQ foi avaliada também. Neste sentido, células dendríticas (DCs) diferenciadas a partir de precursores de medula óssea foram tratadas com PQ e avaliadas quanto ao seu perfil fenotípico e funcional. Observou-se uma redução na expressão de marcadores de maturação de DCs tratadas com PQ (DC-PQ) em comparação às células não tratadas (DC-PBS). A transferência adotiva de DC-PQ resultou na redução do quadro clínico de EAE. Os resultados obtidos nesse trabalho permitem concluir que a primaquina é um fármaco eficaz na atenuação dos sintomas da EAE por meio da modulação de componentes celulares e moleculares do sistema imune<br>Abstract: Multiple sclerosis (MS) is an autoimmune chronic inflammatory disease that affects the central nervous system (CNS) causing neurological disorders arised from axonal demyelination, particularly in the white matter of the CNS organs. The disease affects more than 2 million people worldwide and still has no cure. The successfully used therapeutic approaches consist in the application of monoclonal antibodies, immunomodulatory cytokines and anti-inflammatory drugs. Still, such strategies are dependent on expensive and toxic drugs. The use of antimalarial drugs in the treatment of experimental autoimmune encephalomyelitis (EAE, experimental model of MS), such as chloroquine and dihydroartemisinin, has shown promising results in attenuation of the clinical signs of mice; however, the toxic effects of these substances are an important limiting factor for clinical use. In this sense, this study aimed to characterize the therapeutic effects of primaquine (PQ), an antimalarial drug analog to chloroquine but with reduced toxicity, in EAE in C57BL / 6 mice. To this end, mice were treated with PQ intraperitoneally (i.p.) for five consecutive days, and the effects of direct administration were evaluated on spleen T lymphocyte subpopulations. Similarly, mice bearing EAE were treated with PQ as above, and disease development was evaluated. The results showed a significant reduction in the severity of EAE in mice treated with primaquine compared to animals in the control group. Amelioration of the clinical signs was correlated with (i) an increase in gene expression of anti-inflammatory cytokines and decrease in gene expression of inflammatory cytokines, (ii) reduction in microglia activation and (iii) the decreased CNS glial reactivity in mice treated with PQ compared to untreated group. There was also an increase in the frequency of regulatory T cells in the spleens of mice treated with PQ. Subsequently, regulatory T cells (Tregs, CD4+CD25+ ) and effector T cells (CD4+CD25-) were isolated from spleens of mice treated with PQ, and adoptively transferred to mice with EAE. It was observed a reduction in the severity of EAE in mice recipients of Treg cells compared to mice recipients of effector T cells. Similarly to what was observed in mice directly treated with PQ, the lower severity of EAE was correlated with a reduction in the expression of inflammatory mediators and glial reactivity in the CNS. The immunosuppressive capacity of PQ was evaluated as well. In this regard, dendritic cells (DCs) differentiated from bone marrow precursors were treated with PQ and assessed for phenotypic and functional profile. It was observed a reduction in the expression of DC maturation markers treated with PQ (DC-PQ) compared to untreated cells (DC-PBS). The adoptive transfer of DC-PQ resulted in the reduction of the clinical signs of EAE. The results of this work have shown that primaquine is an effective drug in ameliorating the symptoms of EAE through modulation of cellular and molecular components of the immune system<br>Mestrado<br>Imunologia<br>Mestre em Genética e Biologia Molecular

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Basso, Luis Guilherme Mansor. "Interações de fármacos anti-malária com modelos de membrana." Universidade de São Paulo, 2009. http://www.teses.usp.br/teses/disponiveis/76/76131/tde-19032009-113834/.

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Primaquina e cloroquina são agentes antimaláricos amplamente utilizados profilática e terapeuticamente contra esta enfermidade. A interação destes fármacos com sistemas modelo podem fornecer informações úteis no entendimento dos mecanismos envolvidos em sistemas biológicos reais. Neste sentido, através das técnicas de calorimetria diferencial de varredura e ressonância paramagnética eletrônica, estudamos as interações entre os fármacos antimaláricos supracitados e modelos de membrana, no intuito de investigarmos as modificações provocadas por ambos na estrutura lipídica. Os resultados obtidos indicam que a associação da cloroquina com membranas de DMPC em pH fisiológico é limitada. Uma perturbação desta molécula na estrutura e dinâmica lipídica foi detectada apenas numa região próxima ao carbono sete das cadeias acila das fosfatidilcolinas. Os experimentos de DSC mostram que este fármaco tem efeito apenas na diminuição da cooperatividade da transição principal das membranas. Por outro lado, a redução da temperatura de transição de fase lipídica observada nos estudos calorimétricos demonstra que a primaquina promove uma desestabilização da fase gel. Os experimentos de RPE corroboram esse resultado, evidenciado pelo aumento da fluidez da membrana. Adicionalmente, o aumento do empacotamento provocado no centro da bicamada lipídica sugere penetração deste fármaco até esta região. Não foram observadas alterações da estrutura e dinâmica das cadeias lipídicas na fase fluida da membrana. Os resultados obtidos fornecem um melhor entendimento das interações fármacos-lipídios em um nível molecular, que podem ser aplicados no desenvolvimento de sistemas carreadores de ambos os fármacos.<br>Primaquine (PQ) and Chloroquine (CQ) are potent therapeutic agents used in the treatment of malaria. The investigation of drug-lipid interactions is pivotal for understanding their biological activity. Electron Spin Resonance (ESR) and Differential Scanning Calorimetry (DSC) were used to investigate the effects of drug binding on the lipid phase transition and acyl chain dynamics of model membranes made up of 1,2-Dimyristoyl-sn-Glycero-3-Phosphocholine (DMPC) phospholipids. Labels located at different positions along the lipid chain were used to monitor different membrane regions. ESR results indicated that PQ is more effective in changing the membrane structure than CQ. PQ is effective in perturbing the whole chain of DMPC vesicles, whereas the effect of CQ is more pronounced near the polar headgroup region. Furthermore, PQ causes a slight increase of the lipid packing close to the membrane center, suggesting a deeper insertion of this molecule into DMPC bilayers. DSC thermograms revealed that PQ interacts with DMPC decreasing the main transition temperature (TM) by ca. 2ºC and completely abolishing its pre-transition. On the other hand, CQ effects are mainly noticed as a decrease in the cooperativity of the main transition. Because of its lipophilic character, PQ penetrates into the bilayer hydrocarbon region causing considerable disorganization. Electrostatic interaction between CQ and the phosphatidylcholine phosphate groups is probably related with its low membrane permeability. These results shed light on the molecular mechanism of druglipid interaction, which may be useful for the development of lipid drug delivery systems of antimalarial drugs.

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Faria, Dalva Lucia Araujo de. "Investigação espectroquimica de difosfato de cloroquina e de difosfato de primaquina." Universidade de São Paulo, 1991. http://www.teses.usp.br/teses/disponiveis/46/46132/tde-12112014-113312/.

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Difosfato de Primaquina, seu cátion radical e difosfato de Cloroquina foram estudados por espectroscopia no visível/UV, de emissão, vibracional (Raman, IV e IVP) e RPE além de captação de oxigênio, espectroeletroquímica e termogravimetria; um cálculo semiempírico usando o programa MOPAC também foi realizado. Concluiu-se que a forma duplamente protonada do DPQ. é oxidada a um radical que absorve fortemente no visível (552 nm). Tal espécie é altamente reativa e é possível que a principal causa de seu decaimento com o tempo seja a reação com outras moléculas da droga. A forte dependência do espectro eletrônico do DPQ com o pH pode ser atribuído ao aumento na basicidade no estado excitado, o que daria à banda de menor energia do espectro, um certo caráter de transferência de carga interna. Cloroquina foi estudada adsorvida em um eletrodo de prata e pode-se mostrar que a espécie adsorvida é a monoprotonada e que a interação se dá inicialmente pelo átomo de ni trogênio quinolínico mas, à medida em que o potencial é variado ela tende ao posicionamento paralelo à superfície do eletrodo, o que pode ser detectado pelos deslocamentos nas frequências do espectro SER<br>Primaquine diphosphate, its cation radical and chloroquine diphosphate have been studied by vis-UV, emission, vibrational (IR and NIR) and EPR spectroscopy as well as oxygen uptake, spectroelectrochemistry and thermogravimetry; . a semiempirical calculation was performed too. It was shown that the doubly protonated form of DPQ is oxidized to a radical that absorbs in the visible region (552 nm). Such a species is highly reactive and its time decay is mainly due to its interaction with the non-oxidized drug. The strong dependence of the DPQ absorption spectra wi th the pH can be assigned . to a high enhancement of the drug basicity and a certain degree of internal charge transfer occur. Choroquine was studied adsorbed on a silver electrode where it was shown that the adsorption occurs by means of the single protonated form and initially through the quinolinic ni trogen atom but increasing the applied potential i t goes to a flat posi tion what can be inferred from frequencies shifts in the SER spectra

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Fielding, Carole Mary. "Toxic mechanisms of primaquine in erythrocytes and malaria : the oxidant effects of primaquine." Thesis, University of Liverpool, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.316573.

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Ward, S. A. "The biochemical pharmacology of primaquine." Thesis, University of Liverpool, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.354530.

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Braithwaite, Ian Michael. "The hepatic disposition of primaquine." Thesis, University of Liverpool, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.329639.

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Matsutani, Guilherme Costa. "Antimaláricos potenciais: planejamento e síntese de pró-fármacos \"triglicerídicos\" de primaquina (OU) Antimaláricos potenciais: planejamento e síntese de triglicerídios de primaquina." Universidade de São Paulo, 2004. http://www.teses.usp.br/teses/disponiveis/9/9138/tde-27102016-103103/.

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A malária é uma doença que atinge 40% da população mundial e está entre as três maiores doenças infectantes do planeta, juntamente com a AIDS e a tuberculose. As crianças são as principais atingidas, uma vez que se estima que uma criança morra de malária a cada 40 segundos. As principais regiões atingidas são as que relacionam o clima tropical com altos índices de pobreza, como por exemplo a África sub-Sahariana. Este quadro agrava-se com o surgimento de cepas cloroquino-resistentes do Plasmodium falciparum, principal agente causador da malária grave. Muitos dos fármacos aplicados na terapêutica da malária apresentam inúmeros efeitos adversos, baixa biodisponibilidade e alta toxicidade, o que dificulta o emprego na terapêutica. Diante deste quadro urge o desenvolvimento de novos fármacos antimaláricos. A primaquina, fármaco desenvolvido na segunda guerra mundial, é o único esquizonticida tecidual disponível até o momento, porém apresenta baixa biodisponibilidade, em razão da meia-vida curta, e alta toxicidade. Estas características apresentadas pela primaquina podem ser atenuadas com o emprego da latenciação. O trabalho em questão visa ao desenvolvimento de pró-fármacos \"triglicerídicos\', também conhecidos com lipóides. Os pró-fármacos lipóides utilizam a digestão e absorção dos lipídeos para promover absorção, aumentando a biodiponibilidade e tempo de meia-vida, conseqüentemente, diminuindo a toxicidade. Serão sintetizados como transportadores os diglicerídicos dos ácidos palmítico, esteárico e decanóico. Estes ligar-se-ão à primaquina através dos espaçantes succnil, maleil e ftalil.<br>Abstract not available.

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Sousa, Ariane Cavalcante dos Santos. "Síntese de 2,5-diarilfuranos: potenciais sondas fluorescentes usadas como biomarcadores em malária." Universidade de São Paulo, 2016. http://www.teses.usp.br/teses/disponiveis/9/9138/tde-17112016-141313/.

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A malária é uma das principais causas de morte em muitos países de clima tropical, matando mais de 438 mil pessoas anualmente em todo o mundo. Desta forma, o objetivo do presente trabalho foi sintetizar compostos fluorescentes 2,5- diarilfuranos através da reação de acoplamento cruzado tipo Suzuki-Miyaura e acoplar ao fármaco Primaquina para utilizá-los laboratorialmente como biomarcadores específicos, carreadores de substâncias, parasiticidas, além do desenvolvimento de novo método diagnóstico. Através deste tipo de reação, foram sintetizados 3 compostos fluorescentes: a sonda 3-AFA, 3-AFA ala e a 4-AFAPQ. Inicialmente foram utilizadas células primárias, células da linhagem RAW 264.7 e células eritrocíticas, estas provenientes de camundongos Balb/c inoculados pela via intraperitoneal com 106 EI/mL de P. berghei ANKA GFP. Os compostos fluorescentes sintetizados 3-AFA e 3-AFA ala foram incubados com as células acima citadas e verificou-se a capacidade de as sondas penetrarem e marcarem células sadias e/ou infectadas. A aquisição dos resultados foi realizada por meio de citometria de fluxo e microscopia confocal. A partir daí, utilizou-se também sangue humano proveniente de doação que foi infectado com P. falciparum 3D7. A análise dos resultados realizada com microscopia de fluorescência e testes de EC50 com estes eritrócitos, além de células HepG2. As sondas 3-AFA e 4-AFAPQ foram incubadas com estas células para avaliar a ação parasiticida, bem como a citotoxicidade destes compostos. Nossos resultados mostraram que as sondas 3-AFA e 3-AFA ala não foram capazes de penetrar os macrófagos. Entretanto, foram capazes de atravessar a membrana dos eritrócitos infectados marcando o parasita. Quando os compostos 3- AFA e a 4-AFAPQ foram inseridos em eritrócitos humanos infectados pelo P. falciparum 3D7, foi possível observar que ambos marcaram o parasita em suas 3 fases. Mas resultados de EC50 mostraram que os compostos não possuem efeito parasiticida. E podemos concluir que estes compostos não são citotóxicos ás células possuindo então, um potencial em serem estudados mais a fundo, com algumas modificações em suas estruturas para melhorar assim, sua eficiência quanto a seletividade. Diante destes compostos potencialmente fluorescentes, foi possível também desenvolver um novo método de diagnóstico rápido simples e barato que pode possibilitar o alcance em locais aonde os métodos convencionais de microscopia não chegam.<br>Malaria is a major cause of death in many tropical countries, killing over 438 thousand people annually worldwide. Thus, the objective of this study was to synthesize fluorescent compounds 2,5-diarylfuranes through cross-coupling reaction like Suzuki-Miyaura and engage the drug Primaquine to use them as laboratory specific biomarkers, carriers of substances, parasiticide, and the development new diagnostic method. Through this type of reaction, three fluorescent compounds were synthesized: probe 3-AFA, 3-AFA ala and 4-AFAPQ. Initially were used primary cells, strain RAW 264.7 cells line and erythrocytic cells, those derived from Balb/c mice inoculated intraperitoneally with 106 IE/mL of P. berghei ANKA GFP. The synthesized fluorescent compounds 3-AFA and 3-AFA ala were incubated with the above said cells and found the ability of penetrating probes and mark healthy cells and/or infected. The acquisition of the results was performed by flow cytometry and confocal microscopy. From there, it was also used human blood from that donation was infected with P. falciparum 3D7. The analysis performed with fluorescence microscopy and EC50 these tests with erythrocytes, and HepG2 cells. The probes 3-AFA and 4-AFAPQ were incubated with these cells to evaluate the parasiticidal activity and cytotoxicity of these compounds. Our results showed that the probes 3-AFA and 3-AFA ala were not able to penetrate macrophages. However, they were able to pass the membrane of the parasite infected erythrocytes marking. When the fluorescents probes 3-AFA and 4- AFAPQ (coupled Primaquine) were inserted into human erythrocytes infected with P. falciparum 3D7, it was observed that both marked the parasite in her 3 phases. But EC50 results showed that the compounds do not have parasiticidal effect. And we can conclude that these compounds are not cytotoxic to the cells having then a potential be studied further, with some modifications in their structures to improve thus efficiency and selectivity. Given these potentially fluorescent compounds, it was possible to develop a new method of simple and inexpensive rapid diagnosis that can enable the range in places where conventional methods of microscopy not arrive.

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Books on the topic "Primaquin"

1

H, Wernsdorfer Walther, Trigg Peter I, and Special Programme for Research and Training in Tropical Diseases. Scientific Working Group on the Chemotherapy of Malaria., eds. Primaquine: Pharmacokinetics, metabolism, toxicity, and activity : proceedings of a meeting of the Scientific Working Group on the Chemotherapy of Malaria, UNDP/World Bank/WHO Special Programme for Research and Training in Tropical Diseases, held in Geneva, Switzerland, 27-28 February 1984. Published on behalf of the UNDP/World Bank/WHO Special Programme for Research and Training in Tropical Diseases by Wiley, 1987.

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Brondz, Ilia. Historical Overview of Chromatography and Related Techniques in Analysis of Antimalarial Drug Primaquine. Nova Science Publishers, Incorporated, 2011.

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Book chapters on the topic "Primaquin"

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Gooch, Jan W. "Primaquine." In Encyclopedic Dictionary of Polymers. Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_14557.

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Waters, Norman C., and Michael D. Edstein. "8-Aminoquinolines: Primaquine and Tafenoquine." In Treatment and Prevention of Malaria. Springer Basel, 2011. http://dx.doi.org/10.1007/978-3-0346-0480-2_4.

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Childs, Barton, and William H. Zinkham. "The Genetics of Primaquine Sensitivity of the Erythrocytes." In Ciba Foundation Symposium - Regulation of Cell Metabolism. John Wiley & Sons, Ltd, 2008. http://dx.doi.org/10.1002/9780470719145.ch7.

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Childs, Barton, and William H. Zinkham. "The Genetics of Primaquine Sensitivity of the Erythrocytes." In Ciba Foundation Symposium - Biochemistry of Human Genetics. John Wiley & Sons, Ltd, 2008. http://dx.doi.org/10.1002/9780470719152.ch7.

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Baird, J. Kevin, Ari W. Satyagraha, and Germana Bancone. "Glucose-6-Phosphate Dehydrogenase Deficiency and Primaquine Hemolytic Toxicity." In Encyclopedia of Malaria. Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-8757-9_102-1.

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Visser, L. G. "Moet bij reizigers na terugkeer uit een malariagebied primaquine worden voorgeschreven?" In Vademecum permanente nascholing huisartsen. Bohn Stafleu van Loghum, 2006. http://dx.doi.org/10.1007/978-90-313-8808-0_966.

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Silva, José M., and Peter J. O’Brien. "Primaquine-Induced Oxidative Stress in Isolated Hepatocytes as a Result of Reductive Activation." In Advances in Experimental Medicine and Biology. Springer New York, 1991. http://dx.doi.org/10.1007/978-1-4684-5877-0_47.

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"PRIMAQUINE (Primaquine Phosphate)." In Antibiotics Manual. John Wiley & Sons, Ltd, 2017. http://dx.doi.org/10.1002/9781119220787.ch137.

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"Primaquine." In Meyler's Side Effects of Drugs. Elsevier, 2016. http://dx.doi.org/10.1016/b978-0-444-53717-1.01335-4.

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Scholar, Eric. "Primaquine." In xPharm: The Comprehensive Pharmacology Reference. Elsevier, 2007. http://dx.doi.org/10.1016/b978-008055232-3.62458-4.

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Conference papers on the topic "Primaquin"

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Louisa, Melva, Frans D. Suyatna, Septelia Inawati Wanandi, Puji B. S. Asih, and Din Syafruddin. "Intrahepatic transport of primaquine with OCT1: An in vitro study in HepG2 cells." In THE 4TH BIOMEDICAL ENGINEERING’S RECENT PROGRESS IN BIOMATERIALS, DRUGS DEVELOPMENT, HEALTH, AND MEDICAL DEVICES: Proceedings of the International Symposium of Biomedical Engineering (ISBE) 2019. AIP Publishing, 2019. http://dx.doi.org/10.1063/1.5139373.

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Reports on the topic "Primaquin"

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Parshikov, I. A. Biodegradation of Primaquine and the Problem of its Biosafety. ANO RIEPSI, 2019. http://dx.doi.org/10.18411/1995-4417_rnj_62-19.

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Parshikov, Igor, and Evgeny Zaraisky. Possibilities of fungal biodegradation of antimalarial and anticancer primaquine in the environment. Intellectual Archive, 2019. http://dx.doi.org/10.32370/iaj.2262.

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