%0 Journal Article
%T Skin Injuries Reduce Survival and Modulate Corticosterone, C-Reactive Protein, Complement Component 3, IgM, and Prostaglandin E 2 after Whole-Body Reactor-Produced Mixed Field ( -Photons) Irradiation
%A Juliann G. Kiang
%A G. David Ledney
%J Oxidative Medicine and Cellular Longevity
%D 2013
%I Hindawi Publishing Corporation
%R 10.1155/2013/821541
%X Skin injuries such as wounds or burns following whole-body -irradiation (radiation combined injury (RCI)) increase mortality more than whole-body -irradiation alone. Wound-induced decreases in survival after irradiation are triggered by sustained activation of inducible nitric oxide synthase pathways, persistent alteration of cytokine homeostasis, and increased susceptibility to systemic bacterial infection. Among these factors, radiation-induced increases in interleukin-6 (IL-6) concentrations in serum were amplified by skin wound trauma. Herein, the IL-6-induced stress proteins including C-reactive protein (CRP), complement 3 (C3), immunoglobulin M (IgM), and prostaglandin E2 (PGE2) were evaluated after skin injuries given following a mixed radiation environment that might be found after a nuclear incident. In this report, mice received 3£żGy of reactor-produced mixed field ( -photons) radiations at 0.38£żGy/min followed by nonlethal skin wounding or burning. Both wounds and burns reduced survival and increased CRP, C3, and PGE2 in serum after radiation. Decreased IgM production along with an early rise in corticosterone followed by a subsequent decrease was noted for each RCI situation. These results suggest that RCI-induced alterations of corticosterone, CRP, C3, IgM, and PGE2 cause homeostatic imbalance and may contribute to reduced survival. Agents inhibiting these responses may prove to be therapeutic for RCI and improve related survival. 1. Introduction Radiation injuries combined with another trauma were observed at Hiroshima and Nagasaki, Japan, where approximately 60% of victims received radiation alone with approximately 40% of victims having other injuries concurrent with radiation damage [1, 2]. After the Chernobyl reactor meltdown, 10% of 237 victims exposed to radiation received thermal burns [3]. In in vivo experiments with animals including mice [4¨C7], rats [8, 9], guinea pigs [10], dogs [11], and swine [12, 13], burns and wounds usually increase mortality after otherwise nonlethal irradiation. Ionizing radiation perturbs hematopoiesis in bone marrow, which, in turn, depresses the innate immune responses against infectious agents, including production of immunoglobulins, and disturbs the inflammatory responses, including C-reactive protein (CRP), the components of complement, and the normal balance among the inflammatory and anti-inflammatory cytokines and chemokines. Endogenously produced interleukin-6 (IL-6) clearly contributes to the survival of mice recovering from radiation injury [14]. However, the relationship between increases in
%U http://www.hindawi.com/journals/omcl/2013/821541/