Antioxidant compound (E)-2-benzylidene-4-phenyl-1,3-diselenole protects rats against thioacetamide-induced acute hepatotoxicity

Author:

Reis Angélica S.1,Pinz Mikaela P.1,Bortolatto Cristiani F.2,Jesse Cristiano R.3,Savegnago Lucielli1,Roman Silvane4,Luchese Cristiane1,Wilhelm Ethel A.1

Affiliation:

1. Programa de Pós-graduação em Bioquímica e Bioprospecção (PPGBBio), Grupo de Pesquisa em Neurobiotecnologia, Universidade Federal de Pelotas (UFPel), Campus Capão do Leão, Pelotas, CEP 96010-900, RS, Brasil.

2. Laboratório de Síntese, Reatividade e Avaliação Farmacológica e Toxicológica de Organocalcogênios, Universidade Federal de Santa Maria, Santa Maria, CEP 97105-900, RS, Brasil.

3. Universidade Federal do Pampa, Campus Itaqui, Itaqui, CEP 97650-000, RS, Brasil.

4. Universidade Regional Integrada do Alto Uruguai e das Missões Erechim, Fundação Regional Integrada, Ciências da Saúde, Erechim, CEP 99700-000, RS, Brasil.

Abstract

The aim of this study was to investigate whether (E)-2-benzylidene-4-phenyl-1,3-diselenole (BPD) protects against hepatotoxicity induced by thioacetamide (TAA). On the first day of treatment, male adult Wistar rats received BPD (10 or 50 mg·kg–1). On the second day, the rats received a single intraperitoneal injection of TAA (400 mg·kg–1). Twenty-four hours after TAA administration, biochemical determinations and liver histological analysis were carried out. BPD (50 mg·kg–1) reduced plasma aspartate and alanine aminotransferase, alkaline phosphatase, and lactate dehydrogenase activities increased by TAA exposure. Treatment with BPD was effective against increased lipid peroxidation levels and attenuated a decrease in hepatic reduced glutathione and ascorbic acid levels as well as an inhibition of glutathione peroxidase activity caused by TAA exposure. The higher dose of BPD protected against the inhibition of hepatic δ-aminolevulinic dehydratase activity induced by TAA. Finally, histopathological examination of the liver showed that BPD markedly ameliorated TAA-induced hepatic injury. In conclusion, BPD protected against hepatotoxicity and oxidative stress caused by TAA exposure in rats.

Publisher

Canadian Science Publishing

Subject

Physiology (medical),Pharmacology,General Medicine,Physiology

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