Severe ocular alkali burns in rabbits result in a decrease in aqueous humor ascorbate levels to one-third normal levels. If this deficiency is reversed by immediate treatment with parenteral or topical ascorbate, there is a significantly decreased incidence of subsequent corneal ulceration and perforation. The morphologic changes in these ulcerating corneas are typical of those noted in scorbutus (scurvy). It is concluded that alkali injury to the ciliary epithelial transport processes or ciliary body vasculature results in localized deficiency of ascorbic acid in the aqueous humor and cornea. The development of corneal ulceration is thought to be based on this deficiency which results in the failure of fibroblasts to produce sufficient collagen for repair. A randomized clinical trial of ascorbic acid in the treatment of human alkali burned eyes is now underway.