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Titolo:
AN EVALUATION OF RENAL TUBULAR DNA LADDERING IN RESPONSE TO OXYGEN DEPRIVATION AND OXIDANT INJURY
Autore:
IWATA M; MYERSON D; TOROKSTORB B; ZAGER RA;
Indirizzi:
FRED HUTCHINSON CANC RES CTR,1124 COLUMBIA ST SEATTLE WA 98104 FRED HUTCHINSON CANC RES CTR SEATTLE WA 98104 UNIV WASHINGTON,DEPT MED SEATTLE WA 00000 UNIV WASHINGTON,DEPT PATHOL SEATTLE WA 98195
Titolo Testata:
Journal of the American Society of Nephrology
fascicolo: 6, volume: 5, anno: 1994,
pagine: 1307 - 1313
SICI:
1046-6673(1994)5:6<1307:AEORTD>2.0.ZU;2-3
Fonte:
ISI
Lingua:
ENG
Soggetto:
CELL-DEATH; APOPTOSIS; ENDONUCLEASE; FAILURE; ACTIVATION; CALCIUM; DAMAGE; KIDNEY; IRON; RAT;
Keywords:
APOPTOSIS; ENDONUCLEASE; HYDROGEN PEROXIDE; ISCHEMIA; HYPOXIA;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
22
Recensione:
Indirizzi per estratti:
Citazione:
M. Iwata et al., "AN EVALUATION OF RENAL TUBULAR DNA LADDERING IN RESPONSE TO OXYGEN DEPRIVATION AND OXIDANT INJURY", Journal of the American Society of Nephrology, 5(6), 1994, pp. 1307-1313

Abstract

It has recently been suggested that endonuclease activation and/or apoptosis, possibly triggered by oxidant stress, are important pathogenetic mechanisms in oxygen deprivation/reoxygenation-induced proximal tubular cell death. To explore this possibility, DNA ''laddering,'' a characteristic feature of these processes, was sought in: (1) postischemic rat kidneys (25 or 40-min arterial clamping; 0, 1, 4, 8, 24, and 48h and 6 days reflow); (2) posthypoxic isolated rat proximal tubular segments and (3) cultured human kidney proximal tubular cells (HK-2) subjected either to energy depletion plus Ca2+ overload (antimycin A plus 2-deoxyglucose plus Ca2+ ionophore A23187), or to H2O2-induced cell death. DNA was subsequently extracted, electrophoresed through agarosegels, and visualized with ethidium bromide or Southern blotting. To maximize ladder detection, DNA samples were also end-labeled with P-32 dideoxyadenosine triphosphate with terminal deoxynucleotidyl transferase (tdt), followed by electrophoresis. None of the postischemic DNA samples demonstrated any laddering by either ethidium bromide staining or Southern analysis (apoptotic lymphocyte DNA was a positive control). However, trace laddering was apparent by the tdt technique, commencing at 1 h of reflow, peaking at 24 h, and resolving slowly thereafter. This finding correlated with the morphologic expression of tubular necrosis, not apoptosis. Hypoxia/reoxygenation caused proximal tubular segment death (44 to 64%), and HK-2 cells were slowly killed by both theH2O2 and the energy depletion/Ca2+-loading protocols. However, neither protocol induced ethidium bromide- or tdt-detectable DNA laddering. It was concluded that: (1) minimal DNA laddering develops postischemia, and this change is reliably detected only by the tdt method; (2) it correlates with the morphologic expression of tubular necrosis, not apoptosis; and (3) in vitro oxidative- and energy depletion-mediated proximal tubular cell death can be dissociated from DNA ladder formation.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 26/05/20 alle ore 05:38:44