Hydroxylated polychlorinated biphenyls (OH-PCBs) are toxic contaminants produced via biotic or abiotic transformation of PCBs. In this study, we have tested the toxicity of 2,5-dichlorobiphenyl (2,5-DCB) and three of its OH-derivatives, 2'-OH-, 3'-OH-, and 4'-OH-2,5-DCB toward the model plant, Arabidopsis thaliana. Toxicity tests showed that the parent 2,5-DCB (5 mg L −1 ) had little effect on the plants, while all three OH-metabolites (5 mg L −1 ) exhibited a significant toxicity, with 4'-OH-2,5-DCB being the most potent (inhibition concentration 50%-IC 50 in germination tests = 9.8 mg L −1 for 2'-OH-2,5-DCB, 9.5 mg L −1 for 3'-OH-2,5-DCB, and 4.8 mg L −1 for 4'-OH-2,5-DCB). Whole-genome expression microarrays (Affymetrix) showed that exposure to the three OH-PCBs resulted in rather similar expression patterns, which were distinct from the one developing in response to 2,5-DCB. Searching an Arabidopsis microarray database (Genevestigator) revealed that, unlike the parent compound, the three OH-derivatives induced expression profiles similar to inhibitors of brassinosteroid synthesis (i.e., brassinazole, propiconazole, and uniconazole), resulting in severe iron deficiency in exposed plants. Our results suggest that the higher phytotoxicity of OH-derivatives as compared to 2,5-DCB is at least partly explained by the inhibition of the brassinosteroid pathway.