Please use this identifier to cite or link to this item: https://biore.bio.bg.ac.rs/handle/123456789/1074
Title: Ribavirin administration alters ectonucleotidase activities in experimental autoimmune encephalomyelitis
Authors: Lavrnja, Irena
Nedeljković, Nadežda 
Bjelobaba, Ivana
Stojkov, Danijela
Dacić, Sanja 
Pekovic, Sanja
Rakic, Ljubisav
Mostarica-Stojkovic, Marija
Stosic-Grujicic, Stanislava
Stojiljkovic, Mirjana
Keywords: EAE;Ectonucleotidase activity;Rat spinal cord;Ribavirin
Issue Date: 1-Dec-2009
Journal: General Physiology and Biophysics
Abstract: 
The role of extracellular purines and purinoreceptors in the pathophysiology of different neurological disorders is the focus of rapidly expanding area of research. Ectonucleotidases are the enzymes with multiple roles in extracellular nucleotides metabolism and regulation of nucleotidebased intercellular signaling. The aim of present study was to investigate the changes in the ATP, ADP and AMP hydrolyzing activities after ribavirin treatment in spinal cord during experimental autoimmune encephalomyelitis (EAE). Our results demonstrate that ribavirin itself had no significant effect on ectoenzyme activities, when tested in vitro and in vivo on spinal cord crude membrane preparation of intact animals. We observed significant increase in ATP, ADP and AMP hydrolyzing activity in the spinal cord crude membrane preparation in EAE animals at 15 days post immunization compared to control animals. The increase was registered at 28 days post immunization, as well. At same time points, ribavirin treatment decreased ATP, ADP and AMP hydrolyzing activity compared to EAE animals. In addition, no significant changes 8 days post immunization was observed between EAE-induced and ribavirin- treated EAE animals and these levels were similar to control level. Thus, we suppose that ribavirin-induced alteration in ectonucleotidase activities is rather due to its suppression of inflammation, than to its direct action on ATP, ADP and AMP hydrolysis.
URI: https://biore.bio.bg.ac.rs/handle/123456789/1074
ISSN: 0231-5882
Appears in Collections:Journal Article

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