Influence of NADPH oxidase inhibition on oxidative stress parameters in rat hearts

Background: the aim of this study was to assess whether apocynin,an nicotinamide adenine dinucleotide phosphate (nadph) oxidase blocker,influences lipid peroxidation tbars,hydrogen peroxide (h2o2) content,protein level,heart edema,tumor necrosis factor (tnf-a) concentration or the glutathione redox system in heart homogenates obtained from endothelin 1 (et-1)-induced oxidative stress rats. methods: experiments were carried out on adult malewistar-kyoto rats. the animals were divided into 4 groups: group i: salinetreated control; group ii: saline followed by et-1 (3 ?g/kg b.w.,iv); group iii: apocynin (5 mg/kg b.w.,iv) administered half an hour before saline; group iv: apocynin (5 mg/kg b.w.,iv) administered half an hour before et-1 (3 ?g/kg b.w.,iv). results: injection of et-1 alone showed a significant (p < 0.001) increase in thiobarbituric acid reactive substances (tbars) and the hydrogen peroxide level (p < 0.01) vs. control,as well as a decrease (p < 0.001) in the gsh level. apocynin significantly decreased tbars (p < 0.001) and h2o2 (p < 0.05) level (vs. control) as well as improved protein level (p < 0.001) in the heart. apocynin also prevented et-1-induced heart edema (p < 0.05). the presence of et-1 increased the concentration of tnf-a (p < 0.05) while apocynin decreased it (p < 0.05). our results indicate that et-1 may induce oxidative stress in heart tissue by reducing the gsh/gssg ratio,stimulating lipid peroxidation and increasing tnf-a concentration. apocynin diminished these measures of oxidative stress and tnf-a. conclusion: et-1-induced formation of ros in the heart is at least partially regulated via nadph oxidase.