Lipid peroxidation often underlies apoptosis and mitochondrial dysfunction, which are common pathological phenomena in neurodegenerative and lysosomal storage diseases. Graphene quantum dots (GQDs) have garnered considerable interest as a nanomedicine over the last several years due to their biocompatibility and ability to target cellular disorders associated with disease phenotypes. Recent work with cells containing α-synuclein aggregates (i.e., cells mimicking the onset of Parkinson's disease) has demonstrated that GQDs exhibit mitoprotective behavior. In these studies, GQDs were able to permeate the plasma membrane, inhibit mitochondrial deformation, and restore mitochondrial complex I activity. However, the mechanism by which GQDs interacted with mitochondria was neither examined nor understood. It is known that this type of mitochondrial dysfunction is associated with free radical-induced oxidative lipid damage. Therefore, we hypothesize that the observed mitoprotective properties of GQDs arise from the scavenging of reactive oxidative species that would otherwise interact with mitochondrial membranes. To test this hypothesis, we developed a system to examine lipid peroxidation in synthetic membranes while in the presence of GQDs. Here, we used the fluorescent sensor C11-BODIPY to monitor the kinetics of lipid peroxidation in the presence of hydroxyl free radicals. Comparison of peroxidation rates to first principles kinetic models confirmed that GQDs were indeed scavengers of free radicals. When membranes were incubated with GQDs, the lipid peroxidation rate decreased by 90%. Interestingly, when compared to other renowned antioxidants, such as ascorbic acid and Trolox, GQDs exhibited significantly higher antioxidant efficiency. Ascorbic acid and Trolox required substantially higher concentrations than GQDs to achieve comparable levels of reduction to lipid peroxidation rates. These results warrant further investigation of GQDs as a mitochondrial membrane protection agent.