| Abstract [eng] |
Photodynamic treatment (PDT) is used to treat cancer and other diseases caused by cellular overgrowth. The initial damage of PDT is restricted to the site of photosensitiser accumulation. Clinically used photosensitisers show affinity to multiple cellular organelles. We have studied cell response to PDT (apoptosis, autophagy, cell cycle, expression of several genes) mediated by photosensitisers, localised to: 1) mitochondria - 2-(6-amino-3-imino-3H-xanthen-9-yl)benzoic acid methyl ester (Rh123) and 3,7-diamino-2,8-dimethyl-5-phenylphenazinium chloride (Safr); 2) lysosomes - aluminium (III) phthalocyanine tetrasulfonate (AlPcS4); 3) multiple cellular organelles - meso-tetra(3-hydroxyphenyl)chlorin (mTHPC). It was determined that PDT, mediated by Safr, AlPcS4 and mTHPC, induced apoptosis at high cytotoxic dose (CD80), reducing cellular viability for 80%. Medium cytotoxic dose of PDT, mediated by Rh123 and Safr, did not induce cell death, but after Safr-FDP the cell cycle arrest was registered. Medium (CD50) and high (CD80) cytotoxic doses of PDT, mediated by Safr and mTHPC, induced autophagy. The amount of autophagosomes was increased after small, medium and high dose of PDT, mediated by AlPcS4, but the flux through autophagy pathway proceeded only after the small dose (CD20). PDT, mediated by Safr, AlPcS4 or mTHPC, increased the expression of cytokines VEGF-A, IL-1 alpha and transcription factor HIF-1 alpha subunit at the RNA level. |
