Polycyclic aromatic hydrocarbons (PAHs) are phototoxic to animals and plants. To monitor the toxicity of PAHs and understand their mechanism(s) of action, it is important to develop rapid and accurate bioindicators of effect. In this study, we have analyzed the impact of the anthracene photooxidation product, 1,2- dihydroxyanthraquinone (1,2-dhATQ), on mitochondrial electron transport using a preparation of beef heart mitochondria. Employing both NADH and succinate as electron donors, it was found that 1,2-dhATQ inhibited respiratory electron transport to cytochrome c. Using reduced DCPIP (2,6 dichlorophenolindophenol) as an electron donor, it was found that electron transfer was also inhibited. This indicated that inhibition was specific to cytochrome bc1 (ubiquinone-cytochrome c oxidoreductase). Inhibition of cytochrome c oxidase was very weak, indicating that 1,2-dhATQ primarily targets the cytochrome bc1 complex. Thus, analysis of the respiratory electron transport revealed a specific site of impact for 1,2-dhATQ, and a potential mechanistic basis for toxicity of this compound.