Abstract
Photodynamic treatment of murine L929 fibroblasts with hematoporphyrin-derivative causes deterioration of various membrane functions. Most sensitive to photodynamic inactivation are the energy-coupled transport systems for aminoisobutyric acid and for Rb +. The facilitated diffusion system for 2-deoxy- d-glucose is slightly less sensitive. After longer illumination periods also the membrane barrier function is impaired, as reflected by K + leakage and increased passive Rb + uptake. After still longer illumination periods intermolecular protein crosslinking can be observed. This makes it unlikely that intermolecular protein crosslinking is causally involved in the deterioration of these membrane functions.
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