Photodynamic effects induced by meso-tetrakis[4-(carboxymethyleneoxy)phenyl] porphyrin on isolated Sarcoma 180 ascites mitochondria
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Published on: September 17, 2013
S R Chatterjee1, H Possel, T S Srivastava
1Department of Chemistry, Indian Institute of Technology, Powai, Mumbai, India. shampa.chatterjee@medizin.uni-magdeburg.de
Abstract:
Using mitochondria isolated from Sarcoma 180 ascites tumour in Swiss mice as a model system, we have evaluated the ability of a novel porphyrin, meso-tetrakis[4-(carboxymethyleneoxy)phenyl]porphyrin (H2T4CPP), to induce damage on photosensitization. Oxidative damage to mitochondria, one of the primary and crucial targets of the photodynamic effect, is assessed by measuring products of lipid peroxidation such as thiobarbituric acid reactive substances (TBARS) and lipid hydroperoxides (LOOH), besides the loss of activity of the mitochondrial marker enzyme succinate dehydrogenase (SDH). Analysis of product formation, the effect of deuteration and selective inhibition by scavengers of reactive oxygen species (ROS) show that the damage observed is due mainly to singlet oxygen (1O2) and to a minor extent to hydroxyl radicals (.OH). The 1O2 generation and triplet lifetime of this porphyrin have also been estimated. Fluorescence spectroscopy, used to ascertain the binding of this porphyrin to the mitochondrial proteins, shows a rapid association within 0-2 h and a decline thereafter. Confocal microscopy reveals intracellular localisation of this porphyrin in cells in vitro. Our overall results suggest that the porphyrin H2T4CPP, due to its ability to bind to mitochondrial protein components and to generate ROS upon photoexcitation, may have potential applications in photodynamic therapy.
Insights
This study shows that a novel porphyrin, H2T4CPP, causes mitochondrial damage via singlet oxygen and hydroxyl radicals. This porphyrin may be useful in photodynamic therapy.
Area of Science:
- Biochemistry
- Cell Biology
- Photochemistry
Background:
- Mitochondria are key targets in photodynamic therapy.
- Novel photosensitizers are needed to improve therapeutic efficacy.
Purpose of the Study:
- To evaluate the photodynamic damage induced by a novel porphyrin, H2T4CPP, in isolated mitochondria.
- To investigate the mechanisms of damage and the potential of H2T4CPP in photodynamic therapy.
Main Methods:
- Mitochondria isolated from Sarcoma 180 ascites tumor were used.
- Lipid peroxidation products (TBARS, LOOH) and succinate dehydrogenase activity were measured.
- Reactive oxygen species (ROS) generation was analyzed using scavengers and deuteration.
- Porphyrin binding to mitochondrial proteins was assessed using fluorescence spectroscopy.
- Intracellular localization was determined by confocal microscopy.
Main Results:
- H2T4CPP induced oxidative damage to mitochondria upon photosensitization.
- Damage was primarily mediated by singlet oxygen (1O2) and to a lesser extent by hydroxyl radicals (.OH).
- The porphyrin rapidly bound to mitochondrial proteins and localized intracellularly.
Conclusions:
- H2T4CPP effectively generates ROS upon photoexcitation, causing mitochondrial damage.
- The porphyrin's ability to bind mitochondrial proteins suggests potential for targeted photodynamic therapy.
