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The Challenge of Parasite Control
Published in Eric S. Loker, Bruce V. Hofkin, Parasitology, 2023
Eric S. Loker, Bruce V. Hofkin
In other cases, if the gene for a particular membrane receptor experiences a mutation, the receptor may become inactive. If this receptor is ordinarily involved in transporting a specific drug into a parasite, the drug may lose its effectiveness, rendering the parasite resistant. This is believed to be how certain strains of African trypanosomes have developed resistance to diminazene, an important drug used in the treatment of trypanosomiasis in livestock (nagana). To be effective, this drug must enter the parasite and move to the nucleus, where it binds to and interferes with nucleic acid synthesis.
Melarsoprol
Published in M. Lindsay Grayson, Sara E. Cosgrove, Suzanne M. Crowe, M. Lindsay Grayson, William Hope, James S. McCarthy, John Mills, Johan W. Mouton, David L. Paterson, Kucers’ The Use of Antibiotics, 2017
In a recent study of T. brucei rhodesiense isolate from Tanzania, 35 clinical isolates were screened for resistance and 13 were selected for further testing (Kibona et al., 2006). Two were found to show a resistance phenotype in a mouse model and had correspondingly high IC50 and MIC values. These two isolates were also found to be resistant to diminazene, a diamidine drug (related to pentamidine) used to treat animal trypanosomiasis, but not to suramin or isometamidium. Cross-resistance may be explained by mutations in the gene encoding this receptor. However, in a mouse model of druginduced resistance, melarsoprol-induced resistant isolates had lost the TbAT1 gene, whereas the pentamidine-selected population had not (Bernhard et al., 2007). The mechanism of melarsoprol and pentamidine cross-resistance and its frequency has not been fully defined. There is currently no evidence of cross-resistance of melarsoprol to suramin or eflornithine.
Contested Histories
Published in Kevin Bardosh, One Health, 2016
The drugs (notably diminazene aceturate (mostly for chemotherapy), isometamidium chloride (for chemoprophylaxis) and homidium salts (for chemotherapy)) are reasonably effective and relatively easy to administer, and especially as generics very cheap.11 This can be, advocates argue, a livestock owner-led solution, delivered through agro-vets and the private sector drug companies, and so not reliant on large-scale government-led control campaigns, at least for animal trypanosomiasis. A unique mass treatment campaign for cattle has also been used to control the zoonotic parasite in Uganda.12
Could a specific ACE2 activator drug improve the clinical outcome of SARS-CoV-2? A potential pharmacological insight
Published in Expert Review of Clinical Pharmacology, 2020
Lucas A. D. Nicolau, Isabela R. S. G Nolêto, Jand V. R. Medeiros
Diminazene aceturate (Dize: C14H15N7 · 2C4H7NO3; Molecular Weight: 515.5 g/mol; PubChem CID: 5,284,544) is an old antiparasitic used primarily in animal clinical practice that activates ACE2. Dize is an aromatic diamidine that was first described in 1955 and has been originally developed for therapeutic approach in controlling trypanosomiasis, its IUPAC name is 2-acetamido acetic acid; 4-[2-(4-carbami midoylphenyl) iminohydrazinyl] benzene carboximidamide [22]. Nevertheless, in recent years, this drug has been extensively studied with regard to its therapeutic potential and manifold effects; this pleiotropy for pharmacology development has consequently attracted palpable interest in drug repositioning [22]. Actually, several studies have shown that Dize may influence positively other physiological conditions in different tissues ACE2+. In addition to activating ACE2, this drug stimulates the protective axis of the RAS, leading to the cleavage of Ang II. ACE2 metabolizes Ang II to Ang-(1–7) and thus counter regulates the deleterious effects of Ang II [23].
Metal nanoparticles restrict the growth of protozoan parasites
Published in Artificial Cells, Nanomedicine, and Biotechnology, 2018
Oluyomi Stephen Adeyemi, Nthatisi Innocentia Molefe, Oluwakemi Josephine Awakan, Charles Obiora Nwonuma, Omokolade Oluwaseyi Alejolowo, Tomilola Olaolu, Rotdelmwa Filibus Maimako, Keisuke Suganuma, Yongmei Han, Kentaro Kato
Lastly, we sought to evaluate the anti-Trypanosoma efficacy of the NPs in vivo by using a rat model of experimental infection. However, the results were not promising (Figure 7); there was no appreciable decline in the parasite burden for the NP-treated animals compared with the untreated control. Although it appeared that the NPs were trypanostatic, the NP treatments failed to clear the systemic parasite burden and consequently the animals succumbed to their infections in a manner comparable to the fate of the negative drug control group. However, diminazene aceturate treatment (3.5 mg/kg bw) not only reduced the systemic parasite burden but also significantly extended the survival time of the animals.
Evaluation of the non-clinical toxicity of an antiparasitic agent: diminazene aceturate
Published in Drug and Chemical Toxicology, 2022
George Laylson da Silva Oliveira, Ana Paula dos Santos C. L. da Silva
The diminazene aceturate (DIZE; 4-[2-(4-carbamimidoylphenyl) iminohy-drazinyl]benzenecarboximidamide), represented in Figure 1, is the main chemotherapeutic agent used against the protozoan causing trypanosomiasis in animals such as Trypanosoma congolense, Trypanosoma vivax and Trypanosoma brucei (Peregrine 1994, Magona et al.2004, Obi et al. 2013). In addition to its trypanocidal property, diminazene aceturate has also been applied against parasites of the genus Babesia (Mosqueda et al. 2012).