Consulta: creatorFacets:"Sarkis,J.J.F."
Registros recuperados: 5
Data/hora: 01/06/2024 12:30:27

Ectonucleotidase activities in Sertoli cells from immature rats
Provedor de dados: 56
Autores: Casali,E.A.; Silva,T.R. da; Gelain,D.P.; Kaiser,G.R.R.F.; Battastini,A.M.O.; Sarkis,J.J.F.; Bernard,E.A.
Sertoli cells have been shown to be targets for extracellular purines such as ATP and adenosine. These purines evoke responses in Sertoli cells through two subtypes of purinoreceptors, P2Y2 and P A1. The signals to purinoreceptors are usually terminated by the action of ectonucleotidases. To demonstrate these enzymatic activities, we cultured rat Sertoli cells for four days and then used them for different assays. ATP, ADP and AMP hydrolysis was estimated by measuring the Pi released using a colorimetric method. Adenosine deaminase activity (EC 3.5.4.4) was determined by HPLC. The cells were not disrupted after 40 min of incubation and the enzymatic activities were considered to be ectocellularly localized. ATP and ADP hydrolysis was markedly increased by...
Tipo: Info:eu-repo/semantics/article
Palavras-chave: Sertoli cells; Purine nucleotides; ATP diphosphohydrolase; Ecto-5'-nucleotidase; Ectoadenosine deaminase.
Ano: 2001
URL: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2001001000003

Ischemic preconditioning reduces peripheral oxidative damage associated with brain ischemia in rats
Provedor de dados: 56
Autores: Frassetto,S.S.; Schetinger,M.R.C.; Webber,A.; Sarkis,J.J.F.; Netto,C.A.
Brain ischemia followed by reperfusion causes neuronal death related to oxidative damage. Furthermore, it has been reported that subjects suffering from ischemic cerebrovascular disorders exhibit changes in circulating platelet aggregation, a characteristic that might be important for their clinical outcome. In the present investigation we studied tert-butyl hydroperoxide-initiated plasma chemiluminescence and thiol content as measures of peripheral oxidative damage in naive and preconditioned rats submitted to forebrain ischemia produced by the 4-vessel occlusion method. Rats were submitted to 2 or 10 min of global transient forebrain ischemia followed by 60 min or 1, 2, 5, 10 or 30 days of reperfusion. Preconditioned rats were submitted to a 10-min...
Tipo: Info:eu-repo/semantics/article
Palavras-chave: Brain ischemia; Ischemic preconditioning; Oxidative damage; Hydroperoxide-initiated chemiluminescence; Plasma thiols.
Ano: 1999
URL: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X1999001000017

Brain ischemia alters platelet ATP diphosphohydrolase and 5'-nucleotidase activities in naive and preconditioned rats
Provedor de dados: 56
Autores: Frassetto,S.S.; Schetinger,M.R.C.; Schierholt,R.; Webber,A.; Bonan,C.D.; Wyse,A.T.; Dias,R.D.; Netto,C.A.; Sarkis,J.J.F.
The effects of transient forebrain ischemia, reperfusion and ischemic preconditioning on rat blood platelet ATP diphosphohydrolase and 5'-nucleotidase activities were evaluated. Adult Wistar rats were submitted to 2 or 10 min of single ischemic episodes, or to 10 min of ischemia 1 day after a 2-min ischemic episode (ischemic preconditioning) by the four-vessel occlusion method. Rats submitted to single ischemic insults were reperfused for 60 min and for 1, 2, 5, 10 and 30 days after ischemia; preconditioned rats were reperfused for 60 min 1 and 2 days after the long ischemic episode. Brain ischemia (2 or 10 min) inhibited ATP and ADP hydrolysis by platelet ATP diphosphohydrolase. On the other hand, AMP hydrolysis by 5'-nucleotidase was increased after 2,...
Tipo: Info:eu-repo/semantics/article
Palavras-chave: Brain ischemia; Ischemic preconditioning; Rat platelets; ATP diphosphohydrolase; 5'-nucleotidase.
Ano: 2000
URL: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2000001100017

Gadolinium increases the vascular reactivity of rat aortic rings
Provedor de dados: 56
Autores: Angeli,J.K.; Ramos,D.B.; Casali,E.A.; Souza,D.O.G.; Sarkis,J.J.F.; Stefanon,I.; Vassallo,D.V.; Fürstenau,C.R.
Gadolinium (Gd) blocks intra- and extracellular ATP hydrolysis. We determined whether Gd affects vascular reactivity to contractile responses to phenylephrine (PHE) by blocking aortic ectonucleoside triphosphate diphosphohydrolase (E-NTPDase). Wistar rats of both sexes (260-300 g, 23 females, 7 males) were used. Experiments were performed before and after incubation of aortic rings with 3 µM Gd. Concentration-response curves to PHE (0.1 nM to 0.1 mM) were obtained in the presence and absence of endothelium, after incubation with 100 µM L-NAME, 10 µM losartan, or 10 µM enalaprilat. Gd significantly increased the maximum response (control: 72.3 ± 3.5; Gd: 101.3 ± 6.4%) and sensitivity (control: 6.6 ± 0.1; Gd: 10.5 ± 2.8%) to PHE. To investigate the blockade...
Tipo: Info:eu-repo/semantics/article
Palavras-chave: Gadolinium; E-NTPDase; Adenosine; Angiotensin II; AT1receptor.
Ano: 2011
URL: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2011000500010

Catabolism of Ap4A and Ap5A by rat brain synaptosomes
Provedor de dados: 56
Autores: Emanuelli,T.; Bonan,C.D.; Sarkis,J.J.F.; Battastini,A.M.O.
Adenosine 5',5'''-P1,P4-tetraphosphate (Ap4A) and adenosine 5',5'''-P1,P5-pentaphosphate (Ap5A) are stored in and released from rat brain synaptic terminals. In the present study we investigated the hydrolysis of dinucleotides (Ap4A and Ap5A) in synaptosomes from the cerebral cortex of adult rats. Ap4A and Ap5A, but not Ap3A, were hydrolyzed at pH 7.5 in the presence of 20 mM Tris/HCl, 2.0 mM MgCl2, 10 mM glucose and 225 mM sucrose at 37oC. The disappearance of the substrates measured by FPLC on a mono-Q HR column was both time and protein dependent. Since synaptosome integrity was at least 90% at the end of the assay, hydrolysis probably occurred by the action of an ecto-enzyme. Extracellular actions of adenine dinucleotides at central nervous system...
Tipo: Info:eu-repo/semantics/other
Palavras-chave: Ap4A; Ap5A; Diadenosine polyphosphate hydrolase; Brain synaptosomes; ApnAase.
Ano: 1998
URL: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X1998001200003