Uranyl acetate, a suppressor of victorin-induced electrolyte leakage in oat leaves when applied together with, or before, victorin, also suppressed victorin-induced changes in ultrastructure. Uranyl crystallized in cell walls and near the plasmalemma of vascular cells, but was excluded from the protoplasm. Fewer crystals occurred near the plasmalemma when leaves were allowed to take up uranyl and victorin simultaneously than when uranyl alone was absorbed, but deposition in cell wails was similar in the two treatments. No differences in crystal distribution were found in uranyl-treated leaves which subsequently took up either water or victorin. The most striking effect of prolonged exposure to uranyl was increased vesicular activity in the protoplasm, formation of complex concentric membranes, and tonoplast damage. Following victorin treatment, uranyl post-treatment was ineffective in suppressing electrolyte leakage or preserving normal cellular ultrastructure. More severe ultrastructural damage was found in victorintreated leaves after uranyl post-treatments than after posttreatment with water, a result of victorin-induced damage which facilitates uranyl entry into the protoplasm.Alterations in membrane permeability are characteristic of many diseased plant tissues, and these changes may result in secondary metabolic effects on respiration, photosynthesis, hormone activities, and phenolic levels (3,20). Permeability changes in oats (Avena sativa L.) infected with Helminthosporium victoriae are caused by a pathotoxic substance, victorin, secreted by the fungus. The disease is an excellent system for studies on pathological changes in physiology and ultrastructure of plants (13,16,18). The pathotoxin causes loss of electrolytes and labeled compounds from tissues within minutes after treatment of susceptible oat varieties (11,15). The earliest detected ultrastructural change in diseased oats is near the plasmalemma, suggesting that the primary effect of victorin is on plasmalemma permeability (7).Uranyl salts suppressed both blight symptoms and electrolyte leakage in victorin-treated leaves of susceptible oat varieties, but did not prevent victorin-induced inhibition of root growth (4). These compounds are effective whether supplied