Pregled bibliografske jedinice broj: 74170
Kidney ischaemia-reperfusion injury and polyribosome structure
Kidney ischaemia-reperfusion injury and polyribosome structure // Nephron, 89 (2001), 2; 201-207 (međunarodna recenzija, članak, znanstveni)
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Naslov
Kidney ischaemia-reperfusion injury and polyribosome structure
Autori
Pleština, Stjepko ; Gamulin, Stjepan
Izvornik
Nephron (0028-2766) 89
(2001), 2;
201-207
Vrsta, podvrsta i kategorija rada
Radovi u časopisima, članak, znanstveni
Ključne riječi
Kidney; Reperfusion injury; Free radicals; Protein Synthesis; Polyribosome structure
Sažetak
Background: Inhibition of protein synthesis and polyribosome disaggregation are Protein synthesis, 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.
Izvorni jezik
Engleski
Znanstvena područja
Temeljne medicinske znanosti
POVEZANOST RADA
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- Current Contents Connect (CCC)
- Web of Science Core Collection (WoSCC)
- SCI-EXP, SSCI i/ili A&HCI
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