RDH12 codes for a member of the family of short-chain alcohol dehydrogenases/reductases (RDHs) proposed to function in the visual cycle that supplies the chromophore 11-cis retinal to photoreceptor cells. Mutations in RDH12 cause a severe and progressive form of childhood-onset autosomal-recessive retinal dystrophy (arRD), including Leber congenital amaurosis (LCA). We generated Rdh12 knockout mice, which exhibited grossly normal retinal histology at 10 months of age. Levels of all-trans and 11-cis retinoids in dark- and light-adapted animals, and scotopic and photopic electroretinogram (ERG) responses were similar to wild type, as was recovery of the ERG response following bleaching in animals matched for an Rpe65 polymorphism (p.L450M). Lipid peroxidation products and other measures of oxidative stress did not appear to be elevated in Rdh12-/- animals. RDH12 was localized to photoreceptor inner segments and the outer nuclear layer both in mouse and human retina using immunohistochemistry. The present findings suggest that the activity of RDH12 is not rate limiting in the visual response.