Allelopathy, a type of interference competition involving exuded chemicals, has been documented for several types of organisms including terrestrial plants, aquatic macrophytes, microbes, and planktonic algae. However, due to the dynamic nature of the aquatic environment it is unclear whether allelopathy is an evolutionarily stable competition mechanism in such a setting. In this research, we consider a cosmopolitan harmful algae species, Prymnesium parvum, for which multiple ecological roles of its produced deleterious chemicals have been suggested, including broadcast allelopathy (chemicals produced and exuded) and micropredation via cell-cell interactions (chemicals produced and held within the cell). To further investigate the ecological role of the deleterious chemicals, bioassays (with phytoplankton and zooplankton target organisms) were conducted using various fractions of a P. parvum culture grown under balanced N:P stoichiometry or imbalanced, P-reduced stoichiometry. In addition, time-series counts were generated with cell density enumerations and observations of behavior of a mixed species culture at intervals over a 24-h period. Our results suggest that the apparent ecological role of the chemicals in a relatively high-density population shifts depending on system stoichiometry in regard to nitrogen and phosphorus. We show that under balanced N:P conditions, deleterious chemical production is low and cell contact mediates mortality of prey. Differently, under imbalanced, P-reduced conditions chemical effect is high and mass mortality occurs independent of cell contact. Thus, imbalanced N:P ratios shift the apparent ecological role of the deleterious chemicals from one of micropredation to one of broadcast allelopathy. These differences likely influence bloom dynamics and result in different ecological outcomes for systems affected by blooms. Further, we suggest that these differences indicate the importance of predatory mixotrophic feeding in the evolutionary maintenance of deleterious chemical production and the occurrence of allelopathic effects as a byproduct.