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Differential effects of glucose deprivation on the cellular sensitivity towards photodynamic treatment‐based production of reactive oxygen species and apoptosis‐induction
Author(s) -
Kiesslich Tobias,
Plaetzer Kristjan,
Oberdanner Christian Benno,
Berlanda Juergen,
Obermair Franz Josef,
Krammer Barbara
Publication year - 2005
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2004.11.073
Subject(s) - buthionine sulfoximine , glutathione , reactive oxygen species , photodynamic therapy , antioxidant , apoptosis , chemistry , carbohydrate metabolism , photosensitizer , biochemistry , metabolism , glycolysis , intracellular , oxidative stress , programmed cell death , cytotoxicity , microbiology and biotechnology , biology , in vitro , enzyme , photochemistry , organic chemistry
Photodynamic treatment (PDT) employs a photosensitizer and the light‐induced formation of reactive oxygen species – antagonized by cellular antioxidant systems – for the removal of harmful cells. This study addresses the effect of altered carbohydrate metabolism on the cellular antioxidant glutathione system, and the subsequent responses to PDT. It is shown that glucose‐deprivation of 18 h prior to PDT causes a reduced level of intracellular glutathione and an increased cytotoxicity of PDT. These effects can be mimicked by inhibitors of glutathione synthesis (buthionine‐sulfoximine) or its regeneration (1,3‐bis‐(2‐chlorethyl)‐1‐nitrosourea). Inhibited glutathione metabolism shifts the apoptotic window to lower fluences, while glucose deprivation abolishes apoptosis as a result of ATP deficiency. Our results prove evidence for manipulation of the outcome of PDT through internal metabolic pathways.