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环境病理学,毒理学和肿瘤学期刊
影响因子: 1.241 5年影响因子: 1.349 SJR: 0.519 SNIP: 0.613 CiteScore™: 1.61

ISSN 打印: 0731-8898
ISSN 在线: 2162-6537

环境病理学,毒理学和肿瘤学期刊

DOI: 10.1615/JEnvironPatholToxicolOncol.v26.i2.20
pages 75-82

5-Aminolevulinic Acid-Mediated Photodynamic Therapy on Hep-2 and MCF-7c3 Cells

Maria Gabriela Alvarez
Departamento de Biologia Molecular, Facultad de Ciencias Exactas Fisico-Quimicas y Naturales, UNRC, Universidad de Buenos Aires, Argentina
M. S. Lacelli
Departamento de Biologia Molecular, Facultad de Ciencias Exactas Fisico-Quimicas y Naturales, UNRC, Universidad de Buenos Aires, Argentina
Viviana Rivarola
Departamento de Biologia Molecular, Facultad de Ciencias Exactas Fisico-Quimicas y Naturales, UNRC, Universidad de Buenos Aires, Argentina
Alcira Batlle
Centro de Investigaciones sobre Porfirinas y Porfirias (CIPYP), CONICET and University of Buenos Aires, Viamonte 188110A, 1056 Buenos Aires, Argentina
Haydee Fukuda
Centro de Investigaciones sobre Porfirinas y Porfirias (CIPYP), CONICET, FCEN-University of Buenos Aires, Viamonte 188110A, 1056 Buenos Aires, Argentina

ABSTRACT

The cytotoxic effect of 5-aminolevulinic acid (ALA) induced protoporphyrin IX (PPIX) on two human carcinoma cell lines, MCF-7c3 cells and Hep 2 cells, was studied. In both cell lines, PPIX content depends on the ALA concentration and incubation time. The maximal PPIX content was higher in the MCF-7c3 cells, reaching a value of 8 μg/106 cells, compared to the Hep-2 cells, which accumulated 3.2 μg/106 cells. Treatment of cells with the iron chelator desferrioxamine prior to ALA exposure enhances the amount of PPIX, consequently diminishing enzymatic activity of ferroquelatase. Photo sensitization of the cells was in correlation with the PPIX content; therefore, conditions leading to 80% cell death in the MCF-7c3 cells provoke a 50% cell death in the Hep 2 cells. Using fluorescence microscopy, cell morphology was analyzed after incubation with 1 mM ALA during 5 hr and irradiation with 54 Jcm−2; 24 hr post-PDT, MCF-7c3 cells revealed the typical morphological changes of necrosis. Under the same conditions, Hep-2 cells produced chromatine fragmentation characteristic of apoptosis. PPIX accumulation was observed to occur in a perinuclear region in the MCF-7c3 cells; while in Hep-2 cells, it was localized in lysosomes. Different mechanisms of cell death were observed in both cell lines, depending on the different intracellular localization of PPIX.


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