Is arachidonic acid an endoschistosomicide?
Autor: | Azza M. Gawish, Hatem Tallima, Marwa Abou El-Dahab, Rashika El Ridi, Violette Said Hanna |
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Jazyk: | angličtina |
Rok vydání: | 2018 |
Předmět: |
0301 basic medicine
030231 tropical medicine Hamster Microbiology 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine In vivo parasitic diseases Oil Red O lcsh:Science (General) Schistosoma haematobium lcsh:R5-920 Multidisciplinary biology Schistosoma mansoni biology.organism_classification Immunohistochemistry In vitro 030104 developmental biology chemistry Arachidonic acid Rat schistosomiasis biology.protein Oil Red O staining Antibody lcsh:Medicine (General) lcsh:Q1-390 Research Article |
Zdroj: | Journal of Advanced Research Journal of Advanced Research, Vol 11, Iss, Pp 81-89 (2018) |
ISSN: | 2090-1224 2090-1232 |
Popis: | Graphical abstract Arachidonic acid interacts with the surface double lipid bilayer shield of larval, developing and adult schistosomes, leading to its disintegration and eventual parasite attrition. Schistosoma mansoni and Schistosoma haematobium are intravascular, parasitic flatworms that infect >250 million people in 70 developing countries, yet not all people of the same community and household are afflicted. Regarding laboratory rodents, mice but not rats are susceptible to infection with S. mansoni and hamsters but not mice are entirely permissive to infection with S. haematobium. A recent Brazilian publication has demonstrated that resistance of the water-rat, Nectomys squamipes to S. mansoni infection might be ascribed to stores of arachidonic acid (ARA)-rich lipids in liver. Several reports have previously shown that ARA is a safe and effective schistosomicide in vitro, and in vivo in mice, hamsters and in children. Schistosoma haematobium appeared more sensitive than S. mansoni to ARA in in vitro and in vivo experiments. Accordingly, it was proposed that ARA increased levels might be predominantly responsible for natural attrition of S. mansoni and S. haematobium in resistant experimental rodents. Therefore, the levels of ARA in serum, lung, and liver of rats (resistant) and mice (susceptible) at 1, 2, 3, 4 and 6 weeks after infection with S. mansoni cercariae and between mice (semi-permissive) and hamster (susceptible) at 1, 2, 3, 4, and 12 weeks after infection with S. haematobium cercariae were compared and contrasted. Neutral triglycerides and ARA levels were assessed in serum using commercially available assays and in liver and lung sections by transmission electron microscopy, Oil Red O staining, and specific anti-ARA antibody-based immunohistochemistry assays. Significant (P |
Databáze: | OpenAIRE |
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