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EFFECTS OF RHODAMINE 123 IN THE DARK AND AFTER IRRADIATION ON MITOCHONDRIAL ENERGY METABOLISM
Author(s) -
Atlante Anna,
Passarella Salvatore,
Moreno Giuliana,
Salet Christian
Publication year - 1992
Publication title -
photochemistry and photobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.818
H-Index - 131
eISSN - 1751-1097
pISSN - 0031-8655
DOI - 10.1111/j.1751-1097.1992.tb02190.x
Subject(s) - irradiation , oxygen , biophysics , singlet oxygen , chemistry , phototoxicity , adenosine triphosphate , mitochondrion , phosphate , electron transport chain , phosphorylation , atp hydrolysis , oxidative phosphorylation , metabolism , photochemistry , rhodamine 123 , atp synthase , rhodamine , biochemistry , atpase , fluorescence , biology , physics , organic chemistry , multiple drug resistance , nuclear physics , in vitro , enzyme , antibiotics , quantum mechanics
— Isolated rat liver mitochondria have been used to study the mechanism of toxicity of Rhodamine 123 (Rho 123) in the dark and after irradiation with visible light. We report an inhibition of adenosine 5′‐diphosphate phosphorylation which is increased after illumination. In the dark, the first steps of the phosphorylation process ( i.e . the entry of substrates into the matrix, the electron transport to oxygen and the creation of the proton gradient) as well as ATPase activity are not significantly perturbed at Rho 123 concentration below 10 μg/mL. In contrast, the movements of the phosphate compounds are drastically impaired. Irradiation strengthens the detrimental effects in an oxygen dependent process. The nature of the noxious transient species is not clearly established, but it is suggested that singlet oxygen could be responsible for the observed damage.

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