Oxine and copper oxinate have a long history of use as fungicides. Ability to chelate and lipophilicity have been regarded as essential to the action of oxine. The most widely held hypothesis on the mechanism of action of oxine holds that oxine is only active when it can form saturated chelates with metals in the medium which enter the cell and dissociate to liberate a toxic half-chelate. Metals, chelating molecules and pH were investigated for their effect on the fungitoxicity of oxine and copper oxinate. Oxine fungitoxicity increased with increase in medium pH, inhibitory activity corresponding most closely with the concentration of the neutral species. Chelation of oxine with metals in the medium was found not to be a requirement for oxine fungitoxicity. Potentiation of the action of oxine by metals is explained by the formation of more fungitoxic and soluble metal oxinates and antagonism by the formation of less soluble or less active metal oxinates. Chelating amino acids, nucleic acid bases and EDTA did not antagonize oxine fungitoxicity. Antagonism by riboflavin and folic acid suggests interaction of oxine with specific cellular functions in fungi. The fungitoxicity of copper oxinate was generally not affected by metals, chelating molecules or changes in medium pH. It is proposed that the data support the inherent fungitoxicity of oxine, the role of metal oxinates as co-toxicants and independent mechanisms of action for oxine and copper oxinate.