Fiche publication
Date publication
avril 2016
Journal
Aquatic toxicology (Amsterdam, Netherlands)
Auteurs
Membres identifiés du Cancéropôle Est :
Dr GIANGRANDE Angela
Tous les auteurs :
Hollmann G, Linden R, Giangrande A, Allodi S
Lien Pubmed
Résumé
Ultraviolet (UV) radiation can produce biological damage, leading the cell to apoptosis by the p53 pathway. This study evaluated some molecular markers of the apoptosis pathway induced by UVA, UVB and UVA+ UVB (Solar Simulator, SIM) in environmental doses, during five consecutive days of exposure, in the brain of the crab Ucides cordatus. We evaluated the central nervous system (CNS) by immunoblotting the content of proteins p53, p21, phosphorylated AKT, BDNF, GDNF, activated caspase-3 (C3) and phosphohistone H3 (PH3); and by immunohistochemical tests of the cells labeled for PH3 and C3. After the fifth day of exposure, UVB radiation and SIM increased the protein content of p53, increasing the content of AKT and, somehow, blocking p21, increasing the content of activated caspase-3, which led the cells to apoptosis. The signs of death affected the increase in neurotrophins, such as BDNF and GDNF, stimulating the apoptotic cascade of events. Immunohistochemical assays and immunoblotting showed that apoptosis was present in the brains of all UV groups, while the number of mitotic cells in the same groups decreased. In conclusion, environmental doses of UV can cause apoptosis by increasing p53 and decreasing p21, revealing an UV-damage pathway for U. cordatus.
Mots clés
Animals, Apoptosis, genetics, Arthropod Proteins, genetics, Brachyura, radiation effects, Cyclin-Dependent Kinase Inhibitor p21, genetics, Gene Expression Regulation, Nervous System, radiation effects, Sunlight, Tumor Suppressor Protein p53, genetics, Ultraviolet Rays, Water Pollutants, Chemical, toxicity
Référence
Aquat. Toxicol.. 2016 Apr;173:1-8
