Effect of Steroid on Mitochondrial Oxidative Stress Enzymes, Intestinal Microflora, and Bacterial Translocation in Rats Subjected to Temporary Liver Inflow Occlusion

Department of General Surgery, Inonu University Turgut Ozal Medical Center, School of Medicine, Malatya, Turkey.
Transplantation Proceedings (Impact Factor: 0.98). 04/2006; 38(2):378-81. DOI: 10.1016/j.transproceed.2006.01.018
Source: PubMed


Protective effects of steroids against ischemia-reperfusion (I/R) injury are well known, but there is little information about the influence of temporary inflow occlusion on intestinal barrier function or bacterial translocation. The aim of this experimental study was to investigate the effects on liver, kidney, spleen, ileal mitochondrial stress enzymes, and bacterial translocation of methylprednisolone (MP) in rats undergoing temporary liver inflow occlusion. Twenty-seven pathogen-free Wistar albino rats were randomized into three groups: group A: I/R (n = 10); group B: I/R + MP (n = 10); and group C: sham (n = 7). Rats in groups A and B were subjected to 20 minutes of portal vein and hepatic artery occlusion with 3 mg/kg MP injected into group B animals intraperitoneally during the occlusion. Twenty-two hours later, all rats were sacrificed to measure mitochondrial oxidative stress enzymes in liver, kidney, spleen, and ileum. We evaluated intestinal bacterial counts, intestinal mucosal histopathology, bacterial translocation to mesenteric lymph nodes (MLN), liver, spleen, and kidney. Decreased levels of malondialdehyde and increased levels of glutathione were observed in all examined tissues of group B compared to those of group A rats. Statistically significant increases in the intestinal counts of Klebsiella spp and Proteus spp and of bacterial translocation to liver, kidney, spleen, and MLN were measured in group B with respect to group A.

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    • "This fact may be regarded as a hint that other mechanisms outside XO inhibition are responsible for the protective effect of allopurinol in liver I/R injury (Jaeschke, 1991). Steroids and non-steroid anti-inflammatory drugs (NSAID) have been reported to inhibit superoxide production and moreover NSAID can impede ROS production from arachidonic acid by inhibiting cycloxygenase (Kirimlioglu et al., 2006). Cycloxygenase (COX) is a key enzyme in the arachidonic acid cascade which induces the formation of prostaglandin E2 (PGE2). "
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    ABSTRACT: Hepatic ischemia/reperfusion (I/R) injury consists of a sequel of cellular and humoral events that finally leads to parenchymal and nonparenchymal cell death. It is of utmost importance as regards the outcome of liver transplantation and liver resections. There is ample evidence that the key role in the inflicted injury is ascribed to reactive oxygen species (ROS) generated mainly by Kupffer cells and neutrophils during reperfusion, with the participation of endothelial cells and hepatocytes. ROS can procure serious damage to cellular membranes and genomic material. The disaster culminates with the initiation of several inflammatory mediators. On the other hand, cells posses a very potent, enzymatic and non enzymatic antioxidant system capable to mitigate oxidant stress or scavenge ROS, thus preserving to some extent cellular redox state. When the imbalance between oxidant stress and antioxidant systems predominates, cell death ensues. The spectre of liver I/R injury therapeutic options includes a plethora of antioxidant agents, natural or synthetic, and extends to genetic modifications. The aim of this article is to review the current knowledge on the generation and mode of action of ROS and to give a further insight on the antioxidant compounds that comprise the therapeutic quiver of this complicated syndrome.
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    ABSTRACT: Liver ischemia-reperfusion injury occurs in a number of clinical settings, including liver surgery, transplantation, and circulatory shock, leading to significant morbidity and mortality. There is a substantial evidence that hepatic ischemia-reperfusion injury results from an intense inflammatory response initiated by oxidative stress in the liver parenchyma during reperfusion. The anti-inflammatory effects of glucocorticosteroids (GCs) have been known for decades and have found extensive therapeutic use in a wide range of clinical situations associated with organ ischemia. Based on their biological effects, routine perioperative GCs administration has been advocated to reduce hepatic ischemic injury. However, the use of GCs in hepatic surgery remains controversial and clinical benefits are still uncertain. The aim of this review is to present the experimental and clinical evidence about the role of GCs in modulating hepatic ischemia-reperfusion injury.
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