Abstract
Exposure to high dose radiation causes to radiation injury. There are many reports that radiation activates the production of tumor necrosis factor α (TNFα) in various cells including monocytes/macrophages and granulocytes. TNF α is also considered to be a proinflammatory cytokine and this factor plays a critical role in the initiation and continuation of inflammation and immunity. The excess production of TNFα leads to damage of organs. However, the role(s) of TNFα is not fully understood in radiation exposure. In this study, we investigated the roles of TNFα in mice exposed to radiation. We compared the wild-type (TNFα+/+) and the knockout (TNFα-/-) BALB/c mice. Both mice were subjected to γ-ray radiation at a dose of 5-7 Gy. The survival durations in TNFα-/- mice were shorter than in TNFα+/+ mice. The survival rate in TNFα+/+ mice exposed to 5 Gy was almost 95, 90 and 65% on days 5, 10, and 30 after radiation, respectively. On the other hand, those in TNFα-/- mice were about 75, 35 and 15%. In order to investigate the cause of death, we compared weights of body and organs, the numbers of surviving intestinal crypts, apoptosis in crypts, liver function including plasma ALT, AST, or ALP level, and numbers of blood cells following radiation. We also performed histo-pathological study. However, there was no significant difference between TNFα+/+ and TNFα-/- mice. Our results from TNFα-/- mice suggest that TNFα plays an important role in the radiation exposure, whereas the cause of death in TNFα-/- mice exposed to radiation. Further studies are in progress.
