OBJECTIVES: In this study, the antioxidant action of ((4-tert-butylcyclohexylidene) methyl) (4-methoxystyryl) sulfide, a novel unsymmetrical divinyl sulfide, against oxidative damage induced by sodium nitroprusside (SNP) in brains of mice was investigated. METHODS: Mice received SNP (0.335 μmol/site, intracerebroventricular) 30 min after administration of sulfide (10 mg/kg, intragastrically). After 1 h, animals were sacrificed and the brains were removed to biochemistry analysis. Thiobarbituric acid reactive species (TBARS), protein carbonyl (PC) and non-protein thiol (NPSH) levels, as well as catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione reductase (GR) and glutathione S-transferase (GST) activities were determined. KEY FINDINGS: SNP increased TBARS and PC levels, CAT, GPx, GR and GST activities and reduced NPSH levels. Administration of the sulfide attenuated the changes produced by SNP and increased per se GPx activity in brains of mice. Toxicological parameters revealed that this compound did not cause acute renal or hepatic damage. CONCLUSIONS: In conclusion, ((4-tert-butylcyclohexylidene) methyl) (4-methoxystyryl) sulfide protected against oxidative damage caused by SNP in mouse brain. GPx activity is involved, at least in part, in the cerebral antioxidant action of this compound.
OBJECTIVES: In this study, the antioxidant action of ((4-tert-butylcyclohexylidene) methyl) (4-methoxystyryl) sulfide, a novel unsymmetrical divinyl sulfide, against oxidative damage induced by sodium nitroprusside (SNP) in brains of mice was investigated. METHODS:Mice received SNP (0.335 μmol/site, intracerebroventricular) 30 min after administration of sulfide (10 mg/kg, intragastrically). After 1 h, animals were sacrificed and the brains were removed to biochemistry analysis. Thiobarbituric acid reactive species (TBARS), protein carbonyl (PC) and non-protein thiol (NPSH) levels, as well as catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione reductase (GR) and glutathione S-transferase (GST) activities were determined. KEY FINDINGS: SNP increased TBARS and PC levels, CAT, GPx, GR and GST activities and reduced NPSH levels. Administration of the sulfide attenuated the changes produced by SNP and increased per se GPx activity in brains of mice. Toxicological parameters revealed that this compound did not cause acute renal or hepatic damage. CONCLUSIONS: In conclusion, ((4-tert-butylcyclohexylidene) methyl) (4-methoxystyryl) sulfide protected against oxidative damage caused by SNP in mouse brain. GPx activity is involved, at least in part, in the cerebral antioxidant action of this compound.
Authors: Fernanda D da Silva; Mikaela P Pinz; Renata L de Oliveira; Karline C Rodrigues; Francine R Ianiski; Mariana M Bassaco; Claudio C Silveira; Cristiano R Jesse; Silvane S Roman; Ethel A Wilhelm; Cristiane Luchese Journal: Metab Brain Dis Date: 2017-07-14 Impact factor: 3.584
Authors: Renata L de Oliveira; Guilherme T Voss; Jaini J Paltian; Mikaela P Pinz; Marina Laura C P Torres; Michele P Moreira; Marina C Dilelio; Claudio C Silveira; Ethel A Wilhelm; Cristiane Luchese Journal: Metab Brain Dis Date: 2019-06-08 Impact factor: 3.584