Abstract

Aims The effect of telluroacetylenes a–d on pharmacological assays was investigated in vitro. A second objective of this study was to investigate the antioxidant action of compound b against the oxidative damage induced by sodium nitroprusside (SNP) in mouse brain. Main methods In in vitro experiments, lipid peroxidation (LP) and protein carbonyl (PC) levels and δ-aminolevulinate dehydratase (δ-ALA-D) activity were carried out in rat brain homogenate. The thiol peroxidase-like activity and DPPH radical scavenging of telluroacetylenes a–d were investigated. In in vivo experiments, mice received SNP (0.335 µmol per site) intra cerebroventricular (i.c.v.) thirty minutes after oral administration of telluroacetylene b (10 mg/kg). After 1 h, animals were euthanized. The levels of LP and δ-ALA-D, catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR), glutathione S-transferase (GST) activities were carried out in mouse brain homogenate. Key findings Telluroacetylenes a–d, at low μM range, reduced LP and PC levels in rat brain homogenate. Telluroacetylenes a–d showed effect of scavenging DPPH radicals. δ-ALA-D activity was inhibited by telloruacetylenes a–d, at high μM range, in rat brain homogenate. Brains of mice treated with SNP showed an increase in LP and the reduction in δ-ALA-D, GR and GST activities. Telluroacetylene b protected against the oxidative stress caused by SNP in brain of rats. Significance The results support an antioxidant effect of telluroacetylenes a–d in vitro. Telluroacetylene b protected against oxidative damage caused by SNP in mouse brain, suggesting an antioxidant effect of this compound.

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