Reactive oxygen species (ROS) formed by light activated photosensitizers (PSs) are the hallmark of photodynamic therapy (PDT). It is generally accepted that commonly used Pss generate singlet oxygen (O-1(2)) as the cell-toxic species via type II photosensitization. We explored here the consequences of chemical modification and the influence of the net charge of a cationic tetrahydroporphyrin derivative (THPTS) relative to the basic molecular structure on the red-shift of absorption, solubility, mechanistic features, and photochemical as well as cell toxic activity. In order to shed light into the interplay between chemical modification driven intra- and intermolecular photochemistry, intermolecular interaction, and function, a number of different spectroscopic techniques were employed and our experimental studies were accompanied by quantum chemical calculations. Here we show that for THPTS neither O-1(2) nor other toxic ROS (superoxide and hydroxyl energetically feasible and as such observed in acetonitrile). Nevertheless chemically modified tetrapyrrole photosensitizer displays efficient cell toxicity after photoexcitation. The distribution and action of THPTS in rat bladder carcinoma AY27 cells measured with fluorescence lifetime imaging microscopy shows accumulation of the THPTS in lysomes and efficient cell death aftetr irradiation. We found evidence that THPTS (T-1) via efficient electron donors in the biosystems environment and subsequent electron transfer to produce ROS indirectly. These intriguing structure-activity relationships may indeed open new stragegies and avenues in developing PSs and PDT in general.