Abstract
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.