TY - JOUR
T1 - Effects of Organoselenium Compounds on Early and Late Brain Biochemical Alterations in Sepsis-Survivor Rats
AU - Silvestre, Fernanda
AU - Danielski, Lucinéia Gainski
AU - Michels, Monique
AU - Florentino, Drielly
AU - Vieira, Andriele
AU - Souza, Luana
AU - Cardoso, Larissa Colonetti
AU - Schraiber, Rosiane
AU - Rezin, Gislaine Tezza
AU - Vuolo, Francieli
AU - da Rocha, Joao Batista
AU - Barichello, Tatiana
AU - Quevedo, João
AU - Dal-Pizzol, Felipe
AU - Petronilho, Fabricia
N1 - Publisher Copyright:
© 2014, Springer Science+Business Media New York.
PY - 2014/9/23
Y1 - 2014/9/23
N2 - Studies have consistently reported the participation of oxidative stress, energetic metabolism impairment, and creatine kinase (CK) activity alterations in rat brain in early times in an animal model of sepsis and persist for up to 10 days. We have assessed the antioxidant effects of administration of Ebselen (Eb) e diphenyl diselenide (PhSe)2 two organoselenium compounds on brain oxidative stress, energetic metabolism, and CK activity 12, 24 h, and 10 days after sepsis by cecal ligation and perforation (CLP) in rats. Male Wistar rats underwent either sham operation or CLP and were treated with oral injection of Eb (50 mg/kg) or (PhSe)2 (50 mg/kg) or vehicle. 12, 24 h, and 10 days after CLP, the rats were sacrificed, and samples from brain (hippocampus, striatum, cerebellum, prefrontal cortex, and cortex) were obtained and assayed for thiobarbituric acid reactive species and protein carbonyls formation, mitochondrial respiratory chain, and CK activity. We observed in the results a reduction of oxidative damage to lipids and proteins in the different cerebral structures studied and times with the administration of (PhSe)2; however, Eb seems to exert the same effect. Such changes are reflected in the assessment of mitochondrial respiratory chain complexes by reversing the decreased activity of the complex caused by the model of CLP and CK activity. Our data provide the first experimental demonstration that (PhSe)2 was able to reduce the brain dysfunction associated with CLP-induced sepsis in rats, by decreasing oxidative stress parameters mitochondrial dysfunction and CK activity in early times and in late time.
AB - Studies have consistently reported the participation of oxidative stress, energetic metabolism impairment, and creatine kinase (CK) activity alterations in rat brain in early times in an animal model of sepsis and persist for up to 10 days. We have assessed the antioxidant effects of administration of Ebselen (Eb) e diphenyl diselenide (PhSe)2 two organoselenium compounds on brain oxidative stress, energetic metabolism, and CK activity 12, 24 h, and 10 days after sepsis by cecal ligation and perforation (CLP) in rats. Male Wistar rats underwent either sham operation or CLP and were treated with oral injection of Eb (50 mg/kg) or (PhSe)2 (50 mg/kg) or vehicle. 12, 24 h, and 10 days after CLP, the rats were sacrificed, and samples from brain (hippocampus, striatum, cerebellum, prefrontal cortex, and cortex) were obtained and assayed for thiobarbituric acid reactive species and protein carbonyls formation, mitochondrial respiratory chain, and CK activity. We observed in the results a reduction of oxidative damage to lipids and proteins in the different cerebral structures studied and times with the administration of (PhSe)2; however, Eb seems to exert the same effect. Such changes are reflected in the assessment of mitochondrial respiratory chain complexes by reversing the decreased activity of the complex caused by the model of CLP and CK activity. Our data provide the first experimental demonstration that (PhSe)2 was able to reduce the brain dysfunction associated with CLP-induced sepsis in rats, by decreasing oxidative stress parameters mitochondrial dysfunction and CK activity in early times and in late time.
KW - Antioxidants
KW - Brain
KW - Organoselenium compounds
KW - Sepsis
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U2 - 10.1007/s12640-014-9475-y
DO - 10.1007/s12640-014-9475-y
M3 - Article
C2 - 24824533
AN - SCOPUS:84919387873
SN - 1029-8428
VL - 26
SP - 382
EP - 391
JO - Neurotoxicity Research
JF - Neurotoxicity Research
IS - 4
ER -