Oxidative damage induced by hydrogen peroxide is counteracted by the antioxidant enzyme catalase

Abstract

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease that impairs the motor neurons, thus resulting in a progressive inhibition of voluntary muscle movements (Rowland, 2001). Oxidative stress has been established as an essential mechanism in the pathogenesis of ALS (Labo et al., 2010). The aim of this experiment was to induce oxidative stress in the crayfish neuromuscular junction by adding hydrogen peroxide (H₂O₂) to observe the potential antioxidant action of catalase. We first predicted that exposure of the crayfish neuromuscular junction to H₂O₂ would decrease excitatory junction potential (EJP) amplitudes over time. We then hypothesized that upon addition of catalase, the decrease in EJP amplitudes produced due to H₂O₂ exposure would be prevented. The experiment involved isolating the superficial extensor muscle in the crayfish tail, submerging it in solutions of normal saline, H₂O₂, and then H₂O₂ and catalase together. Data collection involved delivery of an electrical impulse to stimulate the nerve innervating a muscle cell and taking intracellular recordings, which could then be used to calculate EJP amplitude. We found that H₂O₂ exposure resulted in a decreased EJP amplitude and catalase successfully prevented this change.