Premium
Bcl‐2 overexpression attenuates dopamine‐induced apoptosis in an immortalized neural cell line by suppressing the production of reactive oxygen species
Author(s) -
Lud Cadet Jean,
Harrington Beverly,
Ordonez Sonia
Publication year - 2000
Publication title -
synapse
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.809
H-Index - 106
eISSN - 1098-2396
pISSN - 0887-4476
DOI - 10.1002/(sici)1098-2396(20000301)35:3<228::aid-syn8>3.0.co;2-#
Subject(s) - reactive oxygen species , apoptosis , immortalised cell line , dopamine , cell culture , chemistry , line (geometry) , microbiology and biotechnology , oxygen , neuroscience , cell , biology , biochemistry , genetics , geometry , mathematics , organic chemistry
Parkinson's disease is a neurodegenerative disease that is consequent to the loss of brain dopamine (DA) cells. These abnormalities are thought, in part, to be a manifestation of increased free radical production during the metabolism of catecholamines. The antiapoptic agent, bcl‐2, has been shown to protect cells against the toxic effects of reactive oxygen species (ROS). Thus, we tested whether bcl‐2 could attenuate the toxic effects of DA on immortalized neural cells. Our results show that DA caused dose‐dependent cell death. The use of confocal microscopy and flow cytometry demonstrated that DA caused cell death through an apoptotic process. Moreover, DA caused a marked increase in ROS in these cells. Furthermore, overexpression of bcl‐2 caused significant protection against DA‐induced apoptosis. These results are discussed in terms of their support for a role of bcl‐2 in the development of Parkinson's disease. Synapse 35:228–233, 2000. © 2000 Wiley‐Liss, Inc.