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A single acute hepatotoxic dose of CCl(4) causes oxidative stress in the rat brain

Carbon tetrachloride (CCl(4)), a hepatotoxic agent is widely used to study the toxic mechanisms in experimental animals. We have investigated whether oxidative stress is induced in the brain at a single hepatotoxic dosage (1 ml/kg bw) of CCl(4). Increased lipid peroxidation (LPO), protein carbonyls...

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Detalles Bibliográficos
Autores principales: Ritesh, K.R., Suganya, A., Dileepkumar, H.V., Rajashekar, Y., Shivanandappa, T.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5598138/
https://www.ncbi.nlm.nih.gov/pubmed/28962426
http://dx.doi.org/10.1016/j.toxrep.2015.05.012
Descripción
Sumario:Carbon tetrachloride (CCl(4)), a hepatotoxic agent is widely used to study the toxic mechanisms in experimental animals. We have investigated whether oxidative stress is induced in the brain at a single hepatotoxic dosage (1 ml/kg bw) of CCl(4). Increased lipid peroxidation (LPO), protein carbonyls (PC) content and glutathione (GSH) depletion were observed in the brain regions of rats treated with CCl(4) which was higher than that of liver. A drastic reduction in the activity of glutathione-S-transferase (GST) was seen in the brain regions which was higher than that of liver. Similarly, activities of glutathione peroxidase (GPx), glutathione reductase (GR), superoxide dismutase (SOD), catalase (CAT), NADH- and NADPH-dehydrogenase were reduced in the brain regions similar to that of liver. Higher induction of oxidative stress in the brain compared to that of liver implies vulnerability of the brain for CCl(4) neurotoxicity. Our study shows that a single hepatotoxic dose of CCl(4) is equally neurotoxic to rats.