Photohemolysis of human erythrocytes sensitized by sulfonated aluminum phthalocyanine was used as an endpoint to study possible chemical modifications of photodynamic therapy. Ascorbate, in concentrations up to 0.1 mM, had a small protective effect. In larger amounts it stimulated the rate of photohemolysis in a concentration dependent manner up to 1mM, by a factor of 2. Azide and D20 tests indicated some participation of singlet oxygen, although to a lesser extent than in the absence of ascorbate. Kinetic considerations augur for a reaction path initiated by an interaction of excited sensitizer-ascorbate, parallel to the singlet oxygen-mediated process. Because of the ubiquitous presence of ascorbate in human tissues in concentrations comparable to those of dissolved oxygen, it is a reasonable estimation that in photodynamic therapy, a fraction of the photodynamic damage proceeds via a Type I, ascorbate-assisted, mechanism. Tocopherol had an effect opposite to that of ascorbate, namely it inhibited the photohemolysis. Likewise, quercetin, a plant flavonoid, was protective against phthalocyanine-induced photohemolysis.