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Titolo:
De novo demonstration and co-localization of free-radical production and apoptosis formation in rat kidney subjected to ischemia/reperfusion
Autore:
Chien, CT; Lee, PH; Chen, CF; Ma, MC; Lai, MK; Hsu, SM;
Indirizzi:
Natl Taiwan Univ, Coll Med, Dept Pathol, Taipei, Taiwan Natl Taiwan Univ Taipei Taiwan v, Coll Med, Dept Pathol, Taipei, Taiwan Natl Taiwan Univ, Coll Med, Dept Surg, Taipei, Taiwan Natl Taiwan Univ Taipei Taiwan niv, Coll Med, Dept Surg, Taipei, Taiwan Natl Taiwan Univ, Coll Med, Dept Physiol, Taipei, Taiwan Natl Taiwan UnivTaipei Taiwan , Coll Med, Dept Physiol, Taipei, Taiwan Natl Taiwan Univ, Coll Med, Dept Urol, Taipei, Taiwan Natl Taiwan Univ Taipei Taiwan niv, Coll Med, Dept Urol, Taipei, Taiwan Natl Taiwan Univ Hosp, Off Med Res Adm, Taipei, Taiwan Natl Taiwan Univ Hosp Taipei Taiwan sp, Off Med Res Adm, Taipei, Taiwan
Titolo Testata:
JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY
fascicolo: 5, volume: 12, anno: 2001,
pagine: 973 - 982
SICI:
1046-6673(200105)12:5<973:DNDACO>2.0.ZU;2-I
Fonte:
ISI
Lingua:
ENG
Soggetto:
PROGRAMMED CELL-DEATH; ACUTE-RENAL-FAILURE; OXIDATIVE STRESS; SUPEROXIDE ANION; CHEMILUMINESCENCE; ISCHEMIA; INJURY; REPERFUSION; GENERATION; INSITU;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
39
Recensione:
Indirizzi per estratti:
Indirizzo: Hsu, SM Natl Taiwan Univ, Coll Med, Dept Pathol, 1-1 Jen Ai Rd, Taipei, Taiwan Natl Taiwan Univ 1-1 Jen Ai Rd Taipei Taiwan Rd, Taipei, Taiwan
Citazione:
C.T. Chien et al., "De novo demonstration and co-localization of free-radical production and apoptosis formation in rat kidney subjected to ischemia/reperfusion", J AM S NEPH, 12(5), 2001, pp. 973-982

Abstract

Ischemia-induced oxidative damage to the reperfused kidney was examined. Amodified chemiluminescence method, an in situ nitro blue tetrazolium perfusion technique, and a DNA fragmentation/apoptosis-related protein assay were adapted for demonstration de novo and co-localization of reactive oxygen species (ROS) production and apoptosis formation in rat kidneys subjected to ischemia/reperfusion injury. The results showed that prolonged ischemia potentiated proapoptotic mechanisms, including increases in the Bax/Bcl-2 ratio, CPP32 expression, and poly-(ADP-ribose)-polymerase fragments, and subsequently resulted in severe apoptosis, including increases in DNA fragmentation and apoptotic cell number in renal proximal tubules (PT) and distal tubules (DT) in a time-dependent manner. The increased level of ROS detected on the renal surface was correlated with that in blood and was intensified by a prolonged interval of ischemia. The main source of ROS synthesis was the PT epithelial cells. The ROS and apoptotic nuclei detected in the PT cells can be ameliorated by superoxide dismutase (SOD) treatment before reperfusion. However, the apoptotic nuclei remained in DT in the SOD-treated rats, indicating that formation of apoptosis in DT was not influenced by the small amounts of ROS produced. in PT and DT cell cultures, significant increases in apoptotic cells and ROS were evident in PT cells after hypoxia/reoxygenation insult. Furthermore, the oxidative damage in PT, bur not in DT, can be alleviated by ROS scavengers SOD and hexa(sulfobutyl)fullerene, confirming that PT are vulnerable to ROS. These results lead us to conclude that ROS produced in significant amounts in PT epithelium under ischemia/reperfusion or hypoxia/reoxygenation conditions may be responsible for the apoptotic death of these cells.

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Documento generato il 07/04/20 alle ore 23:18:28