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 delta-aminolevulinate dehydratase (delta-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 micromol 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 delta-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 muM range, reduced LP and PC levels in rat brain homogenate. Telluroacetylenes a-d showed effect of scavenging DPPH radicals. delta-ALA-D activity was inhibited by telloruacetylenes a-d, at high muM range, in rat brain homogenate. Brains of mice treated with SNP showed an increase in LP and the reduction in delta-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.
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 delta-aminolevulinate dehydratase (delta-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 micromol 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 delta-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 muM range, reduced LP and PC levels in rat brain homogenate. Telluroacetylenes a-d showed effect of scavenging DPPH radicals. delta-ALA-D activity was inhibited by telloruacetylenes a-d, at high muM range, in rat brain homogenate. Brains of mice treated with SNP showed an increase in LP and the reduction in delta-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.
Authors: Daiana S Avila; Dirleise Colle; Priscila Gubert; Aline S Palma; Gustavo Puntel; Flávia Manarin; Simone Noremberg; Paulo C Nascimento; Michael Aschner; João B T Rocha; Félix A A Soares Journal: Toxicol Sci Date: 2010-02-04 Impact factor: 4.849