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Alpha methyl tyrosine inhibits rotenone‐ and staurosporine‐induced apoptosis of adrenal chromaffin cells
Author(s) -
Woodman Ryan,
Lockette Warren
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.747.16
Subject(s) - staurosporine , rotenone , apoptosis , catecholamine , reactive oxygen species , programmed cell death , chemistry , microbiology and biotechnology , biology , pharmacology , endocrinology , medicine , mitochondrion , biochemistry , protein kinase c , kinase
The increased synthesis of catecholamines following traumatic brain injury (TBI) is accompanied by the generation of reactive oxygen species (ROS) that damage neuronal tissues. We hypothesized that inhibition of catecholamine synthesis and ROS formation in catecholamine‐containing neurons with alpha‐methyl tyrosine (AMT) could improve outcome in TBI. Rotenone and staurosporine induce ROS‐dependent apoptosis in adrenal chromaffin cells that synthesize catecholamines. We determined whether or not this inhibitor of catecholamine synthesis could block rotenone‐ and staurosporine‐induced apoptosis of cultured PC12 cells. Cells were incubated for 24 h with either rotenone (10 uM) or staurosporine (0.1 uM), with or without AMT (10 uM); apoptosis was quantified using a luminescent caspase activity assay, and cell viability was determined with cell counts (n = 56 for each intervention, * p < 0.01). AMT significantly reduced rotenone‐ and staurosporine‐induced apoptosis in cultured chromaffin cells and may ameliorate ROS‐induced damage in catecholaminergic neurons. (These studies were supported by Naval Medical Center, San Diego.)