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      Kidney Ischaemia-Reperfusion Injury and Polyribosome Structure



      S. Karger AG

      Kidney, reperfusion injury, Polyribosome structure, Free radicals, Protein synthesis

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          Background: Inhibition of protein synthesis and polyribosome disaggregation are the early events in cell injury provoked by various pathogenic mechanisms, including energy depletion. Polyribosome disaggregation might be expected to occur during ischaemia-reperfusion injury due to ischaemic energy depletion, but also due to detrimental effects of reactive oxygen species on various macromolecules and cellular structures. Methods: Mouse kidney ischaemia-reperfusion injury was provoked by temporary clamping of the renal artery. The polyribosome sedimentation pattern was analyzed by sucrose density centrifugation of kidney postmitochondrial supernatant. Results and Conclusions: Ischaemia for 5 min in the mouse kidney provoked polyribosome disaggregation and an increase of monomer ribosome fraction which was augmented during 10–360 min of reperfusion. Recovery of polyribosome aggregates appeared between 6 and 24 h of reperfusion. Cycloheximide pretreatment prevented only polyribosome disaggregation caused by ischaemia and not that caused by reperfusion. This indicates different mechanisms of polyribosome disaggregation during ischaemia and reperfusion. It probably occurs in the former due to inhibition of initiation of translation, resulting in accumulation of unprogrammed monomer ribosomes, and in the latter due to the splitting of mRNA and breakdown of polyribosomes. Reperfusion did not increase ribonuclease activity in kidney cytosol, but increased the tissue concentration of malonaldehyde, indicating an augmentation in oxygen free radical generation. Possibly these may have caused a non-enzymatic breakdown of polyribosomes. However, pretreatment with allopurinol did not prevent polyribosome breakdown during ischaemia-reperfusion injury.

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          Most cited references 2

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          Reactive oxygen metabolites and reperfusion injury: aberrant triggering of reticuloendothelial function

           G.B. Bulkley (1994)
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            Renal Ischemia – Reperfusion Injury: Contribution of Nitric Oxide and Renal Blood Flow

            The contributions of nitric oxide (NO) and renal blood flow (RBF) were examined in ischemia-reperfusion injury in the rat kidney. The function of both kidneys was assessed by glomerular filtration rate (GFR), and fractional excretion of sodium (FE Na ), calculated before, during unilateral renal artery clamping (45 min), and following reperfusion (90 min). RBF was measured in the same model by ultrasonic flowmetry. Intrarenal NO levels were modulated by administration of S-nitroso-N-acetylpenicillamine (SNAP), L -arginine, acetylcholine, and the NO synthase inhibitor N G -nitro- L -arginine methyl ester ( L -NAME). SNAP increased GFR from 0.20 ± 0.04 ml/min in control ischemic kidney to 0.38 ± 0.06 ml/min and reduced FE Na from 19.3 ± 3.4 to 9.5 ± 1.8%. Similar results were observed when L -arginine was administered. Acetylcholine had no effect on GFR or FE Na . RBF was fully restored within 60 min following reperfusion, with no change in the rate of recovery by L -arginine. L -NAME aggravated the ischemia-reperfusion injury, preventing full restoration of RBF, further reducing GFR and worsening FE Na . In conclusion, ischemia-reperfusion injury ends in low intrarenal levels of NO. We propose that this low NO level results from damage to the endothelial receptor signal transduction process and is not due to impaired NO synthase activity or to changes in RBF.

              Author and article information

              S. Karger AG
              05 September 2001
              : 89
              : 2
              : 201-207
              Department of Pathophysiology, Clinical Hospital Centre Zagreb, University of Zagreb, Croatia
              46068 Nephron 2001;89:201–207
              © 2001 S. Karger AG, Basel

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              Figures: 2, Tables: 5, References: 37, Pages: 7
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