Photodynamic therapy (
PDT) is a treatment modality that utilizes a photosensitizing
drug activated by
laser generated light.
PDT is effective for oncologic applications. Many
cancer patients have undergone a
hematoporphyrin derivative (HpD)-mediated
PDT. The HpD showed a side effect causing prolonged cutaneous photosensitivity. But
ATX-S10, a new
photosensitizer, provides rapid plasma and tissue clearance, comparable photoactivation efficiency, and superior light absorption of visible red. In this study, the
tumor rejection mechanisms of
PDT using
ATX-S10 on HeLa
tumors in nude mice were investigated with morphological and fluorometric methods. The mice were intracutaneously inoculated with HeLa cells, 5 x 10(5) or 1 x 10(7) cells. When
tumors grew to about 10-12 mm in diameter, mice were intraperitoneally administered
ATX-S10, 30 mg/kg, and 2 hours later the
ATX-S10 in
tumors was indirectly measured by a fluorometric machine, PMA-10 (Hamamatsu Photonics K. K.) and the
tumors were irradiated by Optical Parametric Oscillator (Hamamatsu Photonics K. K.) tuned to a wave length at 670 nm, 5 mJ/pulse, 100 J/
tumor. Before and after the irradiation, the effective mechanisms of
PDT with
ATX-S10 were studied by histological and ultrastructural approaches. The results showed occlusive thrombi in the microvasculature of the
tumors and
tumor cell death. These occlusive thrombi were observed within one hour after
PDT at both light and electron microscopy levels, and were more remarkable as time passed after
PDT. Therefore, the morphological studies of
PDT with
ATX-S10 suggested that the rejection mechanisms occurred mainly as a result of the destructive changes of the microvasculature in the
tumors first, and secondly or simultaneously,
tumor cells were destroyed through
necrosis, and finally the
tumors were rejected.