Affiliation: | a Department of Biochemistry and Molecular Biology, The Albany Medical College, Albany, NY 12208, USA b Department of Pediatrics, Albany Medical Center, Albany, NY 12208, USA c Department of Microbiology, Immunology, and Molecular Genetics, The Albany Medical College, Albany, NY 12208, USA d Andrus Gerontology Center, University of Southern California, Los Angeles, CA 90089-0191, USA |
Abstract: | The use of mitochondrial RNA as an indicator of apoptosis was investigated. Exposure of HA-1 fibroblastic cells to 10 H2O2 per 107 cells induced nuclear fragmentation, cell shrinkage, and internucleosomal DNA fragmentation, all characteristics of apoptosis. RNA extracted from control and apoptotic cultures, and analyzed by Northern blot hybridization, revealed a significant increase in the degradation of mitochondrial 16S ribosomal RNA (rRNA) that was associated with apoptosis. Conversely, minimal, if any, degradation of glyceraldehyde-3-phosphate dehydrogenase or actin mRNAs was observed. Similar results were obtained for HA-1 cells treated with the protein kinase inhibitor staurosporine, and for HT-2 T-lymphocytes induced to undergo apoptosis by interleukin-2 withdrawal. In addition, 16S rRNA degradation was an early event that was discernable well before chromatin condensation in hydrogen peroxide-treated HA-1 cells. These observations suggest that degradation of mitochondrial 16S ribosomal RNA is a new marker of mammalian cell apoptosis. © 1997 Elsevier Science Inc. |