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Cell Biology International

Cellular and molecular studies of the initial process of the photodynamic therapy in HEp-2 cells using LED light source and two different photosensitizers

Authors

  • Aline Helena Araujo Machado,

    1. Laboratório de Biologia Celular & Tecidual, UNIVAP, Av Shishima Hifumi 2911, 12244-000 São José dos Campos, SP, Brazil
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  • Pacheco Cristina Soares,

    1. Laboratório de Dinâmica de Compartimentos Intracelulares, UNIVAP, Av Shishima Hifumi 2911, 12244-000 São José dos Campos, SP, Brazil
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  • Newton Soares Da Silva,

    1. Laboratório de Biologia Celular & Tecidual, UNIVAP, Av Shishima Hifumi 2911, 12244-000 São José dos Campos, SP, Brazil
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  • Karen C.M. Moraes

    Corresponding author
    1. Laboratório de Biologia Molecular, Instituto de Pesquisa & Desenvolvimento, UNIVAP, Av Shishima Hifumi 2911, 12244-000 São José dos Campos, SP, Brazil
      Tel.: +55 12 39471132; fax: +55 12 39471149. E-mail addresses: karenmoraes_33@hotmail.com, kamoraes@univap.br
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Tel.: +55 12 39471132; fax: +55 12 39471149. E-mail addresses: karenmoraes_33@hotmail.com, kamoraes@univap.br

Abstract

Photodynamic therapy is an attractive therapeutic procedure for a variety of neoplastic and non-neoplastic disorders that involve a tumor localizing photosensitizer that induces cytotoxicity when activated by a particular wavelength of light. Considering the acceptability of the phthalocyanine photosensitizers, we began to address initial cellular and molecular aspects involved in the therapy that leads to apoptosis or necrosis. After HEp-2 cells had been incubated for 1 h with aluminium tetrasulfonate chloride (AlPcS4) or zinc phthalocyanines (ZnPc) at 10 μM, they were irradiated with an LED prototype (640 nm, 70 mW, 4.5 J/cm2) and subsequently analyzed at 0 and 3 h after the irradiation through MTT, fluorescence microscopy, Annexin V–PI staining and gene transcription analysis. Based on the results we can address that the two photosensitizers led to 2 different death pathways; for AlPcS4, the results suggest an initial process of intrinsic death pathway; and for ZnPc, a prostanoid-mediated activation of death machinery is suggested.

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