Schnyder corneal dystrophy (SCD) is a rare, autosomal, dominantly inherited corneal disorder affecting the central and peripheral cornea and is characterised by cholesterol and phospholipid deposition in the corneal epithelium and stroma, leading to progressive corneal opacification, which may result in glare and disproportionate loss of photopic vision.1–3 Nitric oxide serves as a mediator in diverse and complex cellular processes throughout the eye.4 Increased production of nitric oxide, however, can lead to cytotoxic effects mediated by peroxynitrate, a potent oxidant that finally forms the stable product nitrotyrosine (NT). NT is considered a specific marker for nitrogen-related oxidants; therefore, its presence provides evidence of oxidative damage.5 Malondialdehyde (MDA) is the end product of free-radical–initiated lipid peroxidation, indicating oxygen-dependent degradation of cholesterol and phospholipids.6 7 In view of this evidence, the aim of our study was to examine the possible contribution of the nitric oxide pathway and lipid peroxidation to the pathogenesis of SCD. We examined three eyes from three patients with SCD who underwent a penetrating keratoplasty (PK) in our department (figure 1). The demographic and clinical data of the patients …