Abstract
Tumor necrosis factor α (TNFα) is a pro-inflammatory cytokine that has a wide variety of bioactivities, and over-production of TNFα leads to damages of tissues. TNFα is known to be produced following irradiation in various tissues and anti-TNFα agents have been shown to prevent radiation-induced damage. To determine the role of TNFα in high-dose radiation exposure, we used wild-type (TNFα+/+) and TNFα knockout (TNFα-/-) BALB/c mice. We previously reported that the survival durations in TNFα-/- mice were shorter than those in TNFα+/+ mice after whole body irradiation with 6-6.5 Gy and that administration of recombinant TNFα improved the survival rate in irradiated TNFα-/- mice. Furthermore, the numbers of red blood cells (RBC), the levels of hemoglobin (Hb), the hematocrit values (Ht) and the unsaturated iron binding capacity (UIBC) were significantly lower and the levels of serum iron (Fe) was higher in TNFα-/- mice than TNFα+/+ mice after irradiation. In the present study, we found that administration of recombinant TNFα before irradiation improved the numbers of RBC, Hb levels, Ht values, the Fe levels, and UIBC in irradiated TNFα-/- mice. We also showed that erythroid burst-forming units (BFU-Es) and erythroid colony-forming units (CFU-Es) activities were significantly reduced in TNFα-/- than in TNFα+/+ mice following irradiation, whereas there were no difference in activities of BFU-E and CFU-E between control TNFα+/+ and TNFα-/- mice. Our results suggest that endogenously produced TNFα may play important roles in erythroid hematopoiesis following irradiation.
