Oxidative stress and inducible nitric oxide synthase (iNOS) have been implicated in endothelial cell dysfunction in diabetic retinopathy by formation of peroxynitrite, a cytotoxic product of superoxide and high levels of nitric oxide. Spontaneous diabetic models do not allow for separating the oxidative stress as a result of hyperglycemia from that of the nitric oxide system. in addition chemicals such as streptozotocin which can induce diabetes in animal models cause oxidative stress and induce iNOS before the onset of hyperglycemia. Galactose has been used to induce non-insulin dependent diabetes in mice and rats while gene knockout mice provide a means to study the role of specific NOS components. This study used cytochemical localization of hydrogen peroxide produced by NADH oxidase, a marker for superoxide production, and immunocytochemical localization of nitrotyrosine, a marker for nitric oxide formed radical peroxynitrite, to investigate the role of oxidative stress and the nitric oxide system in galactose induced diabetic retinopathy in iNOS knockout (iNOS%) mice.