Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:1.14.99.3 (heme oxygenase)
 4,196 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Liver injury by 30-min ischemia following reperfusion was examined biochemically and histopathologically. A greater increase in the level of LDH was observed after 1-hr reperfusion. However, the level of LDH decreased in proportion to the period of reperfusion, while the levels of GOT and GPT were also increased rapidly and reached its peak at 12 hr following reperfusion and were almost restored to the control level by 48 hr. A similar increase was obtained in the lipid peroxides of the liver. In addition, cyt. P-450 content and NADPH cyt. c reductase activity decreased in proportion to the period of reperfusion up to 12 hr and then recovered by 96 hr. On the other hand, heme oxygenase activity was significantly increased by ischemia-reperfusion. The ischemia-reperfused liver resulted in various morphological changes with the period of reperfusion. The destruction of Disse's space, vacuolization of the cytoplasm and nonviable hepatocytes were observed after 12-hr reperfusion. These results indicate the greatest damages of the liver induced by 30-min ischemia following reperfusion is observed after 12-hr or 24-hr reperfusion. The liver injury by ischemia-reperfusion could be a useful experimental model to develop for future studies.
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PMID:[An injury of the liver caused by ischemia-reperfusion in rat liver. Report 2: Relationship between the damage of the liver and during the period of reperfusion]. 146 2

Kupffer cells constitute a major source of the heme-degrading enzyme, heme oxygenase (HO). This study examined the roles of Kupffer cells in the modulation of accelerated heme catabolism in ischemia-reperfused rat livers. Livers from rats treated with or without liposome-encapsulated dichloromethylene diphosphonate, a Kupffer cell-depleting reagent, underwent a 20-min ligation of the portal vein followed by reperfusion, The time course of the biliary output of bilirubin, the terminal heme-degrading product, and the expression of HO-1 mRNA and protein were monitored. HO-1 mRNA levels were elevated 3 to 12 h after ischemia/reperfusion in both control and Kupffer cell-depleted rats. Immunohistochemical analyses of control livers revealed that Kupffer cells expressed high levels of HO-1 while its expression in hepatocytes was low. In Kupffer cell-depleted livers, however, periportal hepatocytes displayed marked HO-1 expression. Under these conditions the two groups exhibited distinct profiles of biliary bilirubin excretion. In the controls, total bilirubin excretion increased 8-fold and peaked at 10 h after ischemia/reperfusion. In contrast, the Kupffer cell-depleting treatment resulted in a significant acceleration of the initial rise in bilirubin production, which peaked at 4 h. However, the total amount of bilirubin excreted within the initial 10 h after reperfusion was reduced by 50% as compared with that of the controls. In Kupffer cell-depleted rats, the levels of GOT and GPT as well as serum endotoxin concentrations were elevated after ischemia/reperfusion. These results suggest that Kupffer cells serve as an ischemia/reperfusion sensor that upregulates heme degradation and bilirubin excretion, and that Kupffer cells protect hepatocytes from gut-derived stressers--including endotoxin--following ischemia/reperfusion.
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PMID:The protective role of Kupffer cells in the ischemia-reperfused rat liver. 1238 64

Ischemia/reperfusion (I/R) injury is a multifactorial process that affects liver function after transplantation and resectional surgery. Alterations in hepatic microcirculation and decreased hepatic flow can cause local hypoxia and consequently liver damage, which is worsened by reperfusion. The aim of this study was to evaluate if treatment with L-arginine improved hepatic function in rats with I/R injury. Animals were treated with L-arginine, ischemized for 30 min, and reperfused for 3 h. Plasmatic levels of GOT, GPT, lipid hydroperoxides (LOOH), and total thiol groups (RSH) were evaluated. In addition, we analyzed hepatic LOOH and RSH levels, DNA fragmentation, heme oxygenase 1 (HO-1) expression, and histological modifications. Our results demonstrate a significant improvement in hepatic function of I/R rats compared to the control group. Treatment with L-arginine increased the expression of HO-1. These data suggest that L-arginine could be useful in preventing oxidative damage during hepatic surgery.
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PMID:Heme oxygenase 1 expression in postischemic reperfusion liver damage: effect of L-arginine. 1644 20