The investigation of amifostine(wr-2721)'s effects for oxidative damage in liver tissue after burn trauma

Burn trauma produces significant fluid shifts that reduce cardiac output and tissue perfusion. Aggressive volume replacement to correct hypovolemia and to restore peripheral perfusion increases the oxygen concentration in ischemic tissues. This process exacerbates ischemia-related tissue injury. This injury is more prominent when volume replacement after burn trauma is delayed. Amifostine, an inorganic thiophosphate, is a selective broad-spectrum cytoprotector of normal tissues that provides cytoprotection against ionizing radiation and chemotherapeutic agents. In this experimental study, we aimed to observe the effect of ischemia-reperfusion injury on the liver, which results from early and delayed fluid resuscitation, and amifostine's protective effect on oxidative stress that occurs after burn trauma in liver tissue. Thirtysix female Wistar albino rats were used in this experimental study. Rats were randomly and equally divided into 6 groups. Each group consists of 6 rats. Briefly the characteristics of groups are as follows:Group I: Burn (-) , Amifostine (-) Group II: Burn (-) , Amifostine (+) Group III: Burn (+) , Amifostine (-) ,EFR (Early Fluid Resuscitation) (+) Group IV: Burn (+) , Amifostine (-) ,DFR (Delayed Fluid Resuscitation) (+) Group V: Burn (+) , Amifostine (+) ,EFR (+) Group VI: Burn (+) , Amifostine (+) ,DFR (+) All rats were sacrificed on post burn day 5. We measured liver function tests, TNF- ,IL-6, IL-8 in the samples from portal vein. We also measured malondialdehyde (MDA) as a lipid peroxidation product and glutathione (GSH) as intracellular antioxidant in liver tissue. Both membrane lipid peroxidation and exhausted intracellular defense mechanisms due to oxidative damage in liver tissue after burn trauma were demonstrated in this study too as many other studies previously. We demonstrated both the amifostine had a protective effect against oxidative damage in liver tissue and its beneficial effect on intracellular antioxidant defense mechanisms after burn trauma.