PUVA‐induced apoptosis involves mitochondrial dysfunction caused by the opening of the permeability transition pore

FEBS Letters

Caffieri, Sergio¹  Dall'Acqua, Francesco¹  Di Lisa, Fabio²  Canton, Marcella² 

[1]Dipartimento di Scienze Farmaceutiche, Università di Padova, Padova, Italy

[2]Dipartimento di Chimica Biologica, Università di Padova, Viale Giuseppe Colombo 3, I-35121 Padova, Italy

关键词: Psoralen;    Apoptosis;    Permeability transition;    Mitochondria;    Cyclosporin A;    CsA;    cyclosporin A;    Δψm;    mitochondrial membrane potential;    FCCP;    carbonyl cyanide-p-trifluoromethoxyphenyl-hydrazone;    PI;    propidium iodide;    PARP;    poly(ADP-ribose) polymerase;    PDT;    photodynamic therapy;    POP;    photo-oxidized products of psoralen;    PTP;    mitochondrial permeability transition pore;    PUVA;    psoralen+UVA;    ROS;    reactive oxygen species;    TMRM;    tetramethylrhodamine methyl ester;   

DOI  :  10.1016/S0014-5793(02)02926-5

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

The mechanism of cell death was investigated in Jurkat cells exposed to the combination of psoralen and UVA irradiation (PUVA). Apoptosis was by far prevailing over necrosis and involved mitochondrial dysfunction. The collapse of mitochondrial membrane potential, appears to be caused by the opening of the mitochondrial permeability transition pore since its inhibitor, cyclosporin A, prevented mitochondrial dysfunction and largely attenuated apoptosis. Apoptosis also occurred in cells treated with the photoproducts generated by irradiating psoralen in vitro with an oxygen-dependent process. Thus, the involvement of reactive oxygen species in the onset of PUVA-induced apoptosis appears mostly related to psoralen photooxidation.

【 授权许可】

Unknown