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