NDLI: Acute Brain Damage Induced by Acetaminophen in Mice: Effect of Diphenyl Diselenide on Oxidative Stress and Mitochondrial Dysfunction

Content Provider	Springer Nature Link
Author	Silva, Michele Hinerasky Rosa, Edovando José Flores Carvalho, Nélson Rodrigues Dobrachinski, Fernando Rocha, João Batista Teixeira Mauriz, Jose L. González Gallego, Javier Soares, Félix Alexandre Antunes
Copyright Year	2011
Abstract	Organoselenium compounds exhibit antioxidant activity, as well as a variety of biological activities, with potential pharmacological and therapeutic applications. The aim of this study was to investigate the effect of diphenyl diselenide (PhSe)$_{2}$ in reversing oxidative brain damage and mitochondrial dysfunction caused by administration of acetaminophen (APAP) in mice. Mice received a toxic dose of APAP, followed by a dose of (PhSe)$_{2}$ 1 h later. Four hours after the administration of APAP, plasma was withdrawn from the mice and used for biochemical assays of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) as markers of hepatotoxicity. Brain homogenate was examined to determine oxidative stress. Isolated brain mitochondria were examined to quantify mitochondrial transmembrane's electrical potential and mitochondrial swelling and to estimate reactive oxygen species (ROS) production. APAP administration caused an increase in plasma ALT and AST activities. APAP administration also caused a significant increase in the levels of thiobarbituric acid reactive substances (TBARS) and dichlorofluorescein oxidation in brain homogenate. Similarly, mitochondrial swelling and ROS production increased after APAP administration. APAP treatment also caused a decrease in Na$^{+}$ , K$^{+}$ - ATPase activity and in mitochondrial membrane potential. These alterations observed in the brain of APAP-treated mice were restored by (PhSe)$_{2}$. Glutathione levels were decreased by APAP, but (PhSe)$_{2}$ did not reverse this change. Treatment with (PhSe)$_{2}$ after APAP administration can reverse the neurotoxicity caused by a single toxic dose of APAP. The neuroprotective effect of (PhSe)$_{2}$ is likely associated with its antioxidant properties.
Starting Page	334
Ending Page	344
Page Count	11
File Format	PDF
ISSN	10298428
Journal	Neurotoxicity Research
Volume Number	21
Issue Number	3
e-ISSN	14763524
Language	English
Publisher	Springer-Verlag
Publisher Date	2011-11-12
Publisher Place	New York
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Brain Oxidative stress Mitochondrial dysfunction Organoselenium compounds Acetaminophen Liver damage Pharmacology/Toxicology Cell Biology Neurochemistry Neurobiology Neurology Neurosciences
Content Type	Text
Resource Type	Article
Subject	Neuroscience Toxicology

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