Efeito antioxidante e hepatoprotetor do E-2-benzilideno-4-fenil-1,3- disselenol em um modelo de dano oxidativo induzido por tioacetamida em ratos

Abstract

The liver performs many functions for the homeostasis of the organism, standing out in the control of energy production, immune defense and volume reserve, thus demonstrating an extraordinary functional plurality. However, humans are exposed daily to a variety of compounds that cause damage to liver tissue, such as the use of paints, organic solvents, chemical reagents, fungicides, and exposure to cigarettes. In view of this, it is evident the need to search for therapies that prevent or even reverse the intoxication caused by these compounds. Since oxidative stress is involved in the development and / or maintenance of various pathologies, especially in liver diseases, the use of antioxidant therapies should be considered. In this context, 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) in Wistar rats. On the first day of treatment, the animals received the oral administration of BPD (10 or 50 mg/kg). On the second day, the rats received a single intraperitoneal injection of TAA (400 mg/kg). Twenty-four hours after TAA administration, biochemical determinations and liver histological analysis were carried out. BPD (50 mg/kg) reduced plasma aspartate and alanine aminotransferases, 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 inhibition of hepatic δ-aminolevulinic dehydratase activity induced by TAA was protected by BPD (50 mg/kg). Finally, histopathological examination of 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.