Carboxyfullerenes protect human keratinocytes from ultraviolet-B-induced apoptosis

被引:62
作者
Fumelli, C
Marconi, A
Salvioli, S
Straface, E
Malorni, W
Offidani, AM
Pellicciari, R
Schettini, G
Giannetti, A
Monti, D
Franceschi, C
Pincelli, C
机构
[1] Univ Modena & Reggio Emilia, Dept Neuropsychosensorial Pathol, Dermatol Sect, I-41100 Modena, Italy
[2] Univ Modena & Reggio Emilia, Dept Biomed Sci, Sect Gen Pathol, I-41100 Modena, Italy
[3] Ist Super Sanita, Dept Ultrastruct, I-00161 Rome, Italy
[4] Univ Ancona, Dept Dermatol, Ancona, Italy
[5] Univ Perugia, I-06100 Perugia, Italy
[6] Univ Genoa, Dept Oncol, Natl Canc Inst, Unit Pharmacol & Neurosci, Genoa, Italy
[7] Univ Florence, Dept Pathol & Expt Oncol, Florence, Italy
[8] Univ Bologna, Dept Expt Pathol, I-40126 Bologna, Italy
关键词
apoptosis; carboxyfullerenes; keratinocytes; ultraviolet radiation;
D O I
10.1046/j.1523-1747.2000.00140.x
中图分类号
R75 [皮肤病学与性病学];
学科分类号
100206 ;
摘要
Carboxyfullerene, a water-soluble carboxylic acid derivative of a fullerene, which acts as a free-radical scavenger, was investigated as a protective agent against ultraviolet-light-induced damage in human keratinocytes. First, we demonstrate that carboxyfullerene is not cytotoxic for these cells. In addition, this compound significantly reduces the ultraviolet-B-induced inhibition of keratinocyte proliferation and protects keratinocytes from apoptosis caused by ultraviolet B irradiation in a time- and dose-dependent fashion. Furthermore, the percentage of cells with depolarized mitochondria is significantly lower in ultraviolet-B-irradiated keratinocytes pretreated with carboxyfullerene than in cells provided with diluent alone. Carboxyfullerene also protects human keratinocytes from apoptosis induced by exposure to deoxy-D-ribose, a sugar that causes cell death through a pathway involving oxidative stress. On the other hand, ultraviolet B downregulates bcl-2 levels in human keratinocytes, and carboxyfullerene fails to prevent this effect. These results suggest that carboxy- fullerene protects human keratinocytes from ultraviolet B damage possibly via a mechanism interfering with the generation of reactive oxygen species from depolarized mitochondria without the involvement of bcl-2.
引用
收藏
页码:835 / 841
页数:7
相关论文
共 67 条
[1]   The Bcl-2 protein family: Arbiters of cell survival [J].
Adams, JM ;
Cory, S .
SCIENCE, 1998, 281 (5381) :1322-1326
[2]   D-RIBOSE AND DEOXY-D-RIBOSE INDUCE APOPTOSIS IN HUMAN QUIESCENT PERIPHERAL-BLOOD MONONUCLEAR-CELLS [J].
BARBIERI, D ;
GRASSILLI, E ;
MONTI, D ;
SALVIOLI, S ;
FRANCESCHINI, MG ;
FRANCHINI, A ;
BELLESIA, E ;
SALOMONI, P ;
NEGRO, P ;
CAPRI, M ;
TROIANO, L ;
COSSARIZZA, A ;
FRANCESCHI, C .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1994, 201 (03) :1109-1116
[3]   Ascorbate and alpha-tocopherol prevent apoptosis induced by serum removal independent of Bcl-2 [J].
Barroso, MP ;
GomezDiaz, C ;
LopezLluch, G ;
Malagon, MM ;
Crane, FL ;
Navas, P .
ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS, 1997, 343 (02) :243-248
[4]   1,25-dihydroxyvitamin D-3, transforming growth factor beta 1, calcium, and ultraviolet B radiation induce apoptosis in cultured human keratinocytes [J].
Benassi, L ;
Ottani, D ;
Fantini, F ;
Marconi, A ;
Chiodino, C ;
Giannetti, A ;
Pincelli, C .
JOURNAL OF INVESTIGATIVE DERMATOLOGY, 1997, 109 (03) :276-282
[5]   Successive alteration and recovery of epidermal differentiation and morphogenesis after specific UVB-damages in skin reconstructed in vitro [J].
Bernerd, F ;
Asselineau, D .
DEVELOPMENTAL BIOLOGY, 1997, 183 (02) :123-138
[6]   A ROLE FOR SUNLIGHT IN SKIN-CANCER - UV-INDUCED P53 MUTATIONS IN SQUAMOUS-CELL CARCINOMA [J].
BRASH, DE ;
RUDOLPH, JA ;
SIMON, JA ;
LIN, A ;
MCKENNA, GJ ;
BADEN, HP ;
HALPERIN, AJ ;
PONTEN, J .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1991, 88 (22) :10124-10128
[7]   SKIN PHOTOSENSITIZING AGENTS AND THE ROLE OF REACTIVE OXYGEN SPECIES IN PHOTOAGING [J].
CARBONARE, MD ;
PATHAK, MA .
JOURNAL OF PHOTOCHEMISTRY AND PHOTOBIOLOGY B-BIOLOGY, 1992, 14 (1-2) :105-124
[8]  
Ceruti S, 1997, J NEUROSCI RES, V47, P372, DOI 10.1002/(SICI)1097-4547(19970215)47:4<372::AID-JNR2>3.0.CO
[9]  
2-B
[10]   Oxidative stress mediates synthesis of cytosolic phospholipase A(2) after UVB injury [J].
Chen, X ;
Gresham, A ;
Morrison, A ;
Pentland, AP .
BIOCHIMICA ET BIOPHYSICA ACTA-LIPIDS AND LIPID METABOLISM, 1996, 1299 (01) :23-33