NDLI: Effect of diselenide administration in thioacetamide-induced acute neurological and hepatic failure in mice

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Toxicology Research Vol - 4 Issue - 2

Toxicology Research Vol - 4 Issue - 1

Toxicology Research Vol -3

Toxicology Research Vol -2

Toxicology Research Vol -1

Effect of diselenide administration in thioacetamide-induced acute neurological and hepatic failure in mice

Content Provider	Royal Society of Chemistry (RSC)
Author	Dornelles, Luciano Amaral, Guilherme Pires Schwab, Ricardo S. Soares, Félix Alexandre Antunes Stefanello, Sílvio Terra Dobrachinski, Fernando Bender, Caroline Raquel Carvalho, Nélson Rodrigues de Luz, Sônia Cristina Almeida da Rosa, Edovando José Flores da
Copyright Year	2015
Abstract	Hepatic encephalopathy is a common complication of severe acute hepatic failure and has been associated with high short-term mortality rates. Therefore, the aim of this study was to investigate the effect of diphenyl diselenide (DPDS) and its analogues in protecting against thioacetamide (TAA)-induced acute neurological and hepatic failure in mice. The animals received a TAA dose of 200 mg kg−1 intraperitoneally, and then, 1 hour later, they received 15.6 mg kg−1 of diselenides intraperitoneally. Twenty three hours after diselenide administration, the animals were sacrificed, and blood, brain and liver samples were collected for analysis. The results showed that mice exposed to TAA presented oxidative stress characteristics, such as an increase in lipid peroxidation (LPO), enhanced glutathione peroxidase activity and a decrease in the GSH/GSSH ratio in the brain and liver. In addition, the TAA group showed a decrease in cellular viability in both tissues. TAA treatments also generate reactive oxygen species and cause inhibition of glutathione-S-transferase in liver, which were associated with TAA exacerbated half-life in this tissue. In the histopathological analyses, we observed that TAA induced a large inflammation process that was confirmed according to the elevation of liver myeloperoxidase activity. Moreover, the treatment with diselenides reduced the oxidative stress significantly. Additionally, after the establishment of acute hepatic failure (AHF), DPDS was able to inhibit the inflammatory processes with a more significant decrease in major hepatic damage effects than was presented after treatment with its analogues. Thus, our results showed that DPDS is a promising therapeutic option for the treatment of AHF and hepatic encephalopathy as mice returned to normal conditions after the damage.
Starting Page	707
Ending Page	717
Page Count	11
File Format	HTM / HTML PDF
ISSN	2045452X
Volume Number	4
Issue Number	3
Journal	Toxicology Research
DOI	10.1039/c4tx00166d
Language	English
Publisher	Royal Society of Chemistry
Access Restriction	Open
Subject Keyword	Glutathione peroxidase Oxidative stress The Animals Reactive oxygen species Liver Lipid peroxidation Inflammation Thioacetamide Biological half-life TAA Diphenyl diselenide Myeloperoxidase Glutathione S-transferase Hepatic encephalopathy AHF
Content Type	Text
Resource Type	Article
Subject	Health, Toxicology and Mutagenesis Toxicology

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