Nitric Oxide Protects Mouse Thymocytes from Apoptosis Induced by γ-Irradiation
2001
INTRODUCTION. Nitric Oxide (NO) and its reactive products can either promote or prevent apoptosis depending upon the cell systems and conditions involved (1). We have previously reported that NO-induced mouse thymocyte apoptosis in vitro involves p53 upregulation and caspase-1 activation (2, 3). To further dissect the relationship between NO and thymocyte apoptosis, we investigated the effect of NO on Balb/c thymocytes exposed to γ-irradiation. We found that NO partially protects γ-irradiated thymocytes from apoptosis by preserving mitochondrial integrity and inhibiting caspase activity.
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