1. Antioxidant compound (E)-2-benzylidene-4-phenyl-1,3-diselenole protects rats against thioacetamide-induced acute hepatotoxicity
- Author
-
Cristiani F. Bortolatto, Cristiano Ricardo Jesse, Angélica S. Reis, Lucielli Savegnago, Silvane Souza Roman, Cristiane Luchese, Mikaela P. Pinz, and Ethel A. Wilhelm
- Subjects
Male ,0301 basic medicine ,Antioxidant ,Physiology ,medicine.medical_treatment ,Intraperitoneal injection ,Thioacetamide ,Pharmacology ,medicine.disease_cause ,complex mixtures ,03 medical and health sciences ,chemistry.chemical_compound ,Organoselenium Compounds ,Physiology (medical) ,Lactate dehydrogenase ,mental disorders ,parasitic diseases ,medicine ,Animals ,Rats, Wistar ,General Medicine ,Glutathione ,Ascorbic acid ,digestive system diseases ,Rats ,Oxidative Stress ,030104 developmental biology ,Liver ,chemistry ,Biochemistry ,Alkaline phosphatase ,Lipid Peroxidation ,Oxidative stress - 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.
- Published
- 2017