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Hypericin photosensitization in aqueous model systems

V Senthil1, L R Jones, K Senthil

  • 1Physics Department, Illinois Institute of Technology, Chicago 60616.

Photochemistry and Photobiology
|January 1, 1994
PubMed
Summary
This summary is machine-generated.

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Hypericin photosensitization generates singlet oxygen and superoxide, causing damage to lysozyme and red blood cells. The extent of damage depends on the vehicle, with liposomes showing minimal impact.

Area of Science:

  • Photochemistry
  • Biophysics
  • Biochemistry

Background:

  • Hypericin is a photosensitizer with potential therapeutic applications.
  • Understanding its interaction with biological systems is crucial for optimizing its use.
  • Photosensitization involves the generation of reactive oxygen species (ROS).

Purpose of the Study:

  • To investigate the photosensitization of biological molecules and cells by hypericin.
  • To identify the primary reactive intermediates involved in hypericin photosensitization.
  • To quantify the singlet oxygen quantum yield and assess its dependence on different vehicles.

Main Methods:

  • Photosensitization experiments using lysozyme, liposomes, red blood cells (RBC) ghosts, and intact RBC.
  • Inactivation assays with chemical scavengers (azide ion, 1,4-diazabicyclo(2.2.2)octane, superoxide dismutase).

Related Experiment Videos

  • Lipid peroxidation assays and photohemolysis measurements.
  • Modeling of photohemolysis curves using multihit target theory.

    • Main Results:

    • Singlet oxygen was identified as the major inactivating intermediate for lysozyme, with a contribution from superoxide.
    • The singlet oxygen quantum yield (phi delta) was determined to be 0.49 +/- 0.06.
    • Significant variations in phi delta were observed across different vehicles, with liposomes showing very low values.
    • Hypericin induced lipid peroxidation in liposomes and RBC ghosts, leading to protein cross-linking.
    • Photohemolysis kinetics were dependent on the incubation vehicle, with different 'hit numbers' observed.

    Conclusions:

    • Hypericin photosensitization generates singlet oxygen and superoxide, leading to biomolecular and cellular damage.
    • The efficiency of hypericin as a photosensitizer is highly dependent on the surrounding vehicle.
    • Liposomes, particularly those with saturated lipids, are less susceptible to hypericin-induced photosensitization.
    • The kinetics of red blood cell damage are influenced by the incubation environment.