Antioxidative System in the Liver of Rats Subjected to Combined Irradiation Injury

Until the Chernobyl nuclear plant catastrophe, exposure to radiation combined with other forms of injuries was usually considered as a hazard of nuclear war. The effect of combined irradiation injuries are often defined as the simultaneous effect of irradiation and another noxious stimulus. In our opinion (1) one may talk about combined irradiation injuries (CII) only in the case when the general response of an organism to traumatization is the combination of biological reactions to at least two different etiologic noxious stimuli of which one is irradiation. One of the basic problems of combined injuries in general and CII in particular, is the syndrome of mutual aggravation (SMA) expressed through a very high (potentiated) lethality. The real mechanism(s) of this syndrome is still unknown. In our model of combined irradiation injury, potentiation of irradiation effect was smaller if animals were irradiated in the hypometabolic (“ebb”) compared to the hypermetabolic (“flow”) phase after thermal injury (2). Since the oxygen uptake is greater in the hypermetabolic phase the free radical production is also greater. On the other hand, the transition of hypometabolic to hypermetabolic phase could be analogous to a hypoxia/reoxygenation state. According to Granger et al. (3) this state induces an increase in free radical production. When irradiation injury follows scalding it induces a new flux of free radicals. As a result the antioxidative defense of an organism could be overwhelmed and a disturbance of oxidative-antioxidative processes might occur. Thus, we suppose that overwhelmed antioxidative defense could be the reason for potentiated lethality in combined irradiation injury.