An earlier mechanistic phase of iron toxicity in photosynthetic cells was interpreted in terms of enhanced photodynamic action by the cytochrome b₆/f complex (Cyt b₆/f) via singlet oxygen (¹O₂) on the photosystem II complex (PS II). Iron excess was induced in hydroponically cultured pea (Pisum sativum L.) plants, and its effect on the function of PS II in vivo as well as in vitro was studied under high-irradiance conditions. Iron excess in plants gave rise to a significant increase in Cyt b₆/f content of thylakoids. It appeared that the larger the content of Cyt b₆/f, the more susceptible PS II was to photoinhibition, and the higher the rate of ¹O₂ photoproduction in thylakoids was. The action spectrum for degradation of the D1 protein in thylakoids revealed that photosensitization by nonporphyrin chromophore(s) was apparently associated with near UV to blue light–induced deterioration of PS II. The results are pertinent to the concept that photooxidative damage to PS II, exacerbated by iron accumulation in thylakoid membranes in the form of Cyt b₆/f, is involved in the mechanism of iron toxicity in leaf cells.