Effect of Dexamethasone in Mediating Oxidative Stress Induced by Sodium Nitroprusside on Frog Sciatic Nerve Action Potentials

Abstract

Objective: High concentrations of nitric oxide cause a neurotoxic effect on nerve action potentials. Although glucocorticoids can decrease that effect, the degree of mediation is not known. This study determined the effect of dexamethasone on frog sciatic nerve axon fibers subjected to in vitro oxidative stress.

Methods: Frog sciatic nerves were isolated into Groups: -Control Group-incubation in Ringer's solution; SNP Group-incubation in 10-M-2 sodium nitroprusside solution; SNP+ DEX Group-incubation in 10-M-3 sodium nitroprusside solution followed by incubation in 10-3 M dexamethasone solution; DEX group-incubation in 10-M-3 dexamethasone solution.

Results: In the SNP group, significant changes were observed in the action potential velocity of propagation (p< 0.01), the action potential maximum amplitude (p< 0.01), the slope of the emerging phase (p< 0.01), and the area under the signal curve (p< 0.05). Considering electrophysiological parameters, conduction velocity; maximum amplitude; and signal area values increased above normal by dexamethasone incubation after sodium nitroprusside exposure. In biochemical parameters, the group that received sodium nitroprusside increased the thiobarbituric acid reactive substances (TBARS) concentration (p< 0.001) and decreased superoxide dismutase (SOD) activity (p< 0.01).

Conclusion: Findings supported our hypothesis that dexamethasone reverses damage and decreases oxidative damage to nerve action potential caused by exposure to sodium nitroprusside.