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Titolo:
Effects of myocardial ischemia and reperfusion on mitochondrial function and susceptibility to oxidative stress
Autore:
Venditti, P; Masullo, P; Di Meo, S;
Indirizzi:
Univ Naples Federico II, Dept Gen & Environm Physiol, I-80134 Naples, Italy Univ Naples Federico II Naples Italy I-80134 siol, I-80134 Naples, Italy
Titolo Testata:
CELLULAR AND MOLECULAR LIFE SCIENCES
fascicolo: 10, volume: 58, anno: 2001,
pagine: 1528 - 1537
SICI:
1420-682X(200109)58:10<1528:EOMIAR>2.0.ZU;2-M
Fonte:
ISI
Lingua:
ENG
Soggetto:
RAT-HEART MITOCHONDRIA; NITRIC-OXIDE; FREE-RADICALS; SUBMITOCHONDRIAL PARTICLES; ELECTRON-TRANSPORT; ENERGY-METABOLISM; HYDROGEN-PEROXIDE; GLOBAL-ISCHEMIA; CYTOCHROME-C; OXYGEN;
Keywords:
ischemia-reperfusion; oxidative stress; hydrogen peroxide release; antioxidant capacity; mitochondrial function;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
54
Recensione:
Indirizzi per estratti:
Indirizzo: Di Meo, S Univ Naples Federico II, Dept Gen & Environm Physiol, Via Mezzocannone 8, I-80134 Naples, Italy Univ Naples Federico II Via Mezzocannone 8 Naples Italy I-80134
Citazione:
P. Venditti et al., "Effects of myocardial ischemia and reperfusion on mitochondrial function and susceptibility to oxidative stress", CELL MOL L, 58(10), 2001, pp. 1528-1537

Abstract

We investigated the effects of ischemia duration on the functional response of mitochondria to reperfusion and its relationship with changes in mitochondrial susceptibility to oxidative stress. Mitochondria were isolated from hearts perfused by the Langendorff technique immediately after different periods of global ischemia or reperfusion following such ischemia periods. Rates of O-2 consumption and H2O2 release with complex I- and complex II-linked substrates, lipid peroxidation, overall antioxidant capacity, capacityto remove H2O2, and susceptibility to oxidative stress were determined. The effects of ischemia on some parameters were time dependent so that the changes were greater after 45 than after 20 min of ischemia, or were significantly different to the nonischemic control only after 45 min of ischemia. Thus, succinate-supported state 3 respiration exhibited a significant decrease after 20 min of ischemia and a greater decrease after 45 min, while pyruvate malate-supported respiration showed a significant decrease only after 45 min of ischemia, indicating an ischemia-induced early inhibition of complex II and a late inhibition of complex I. Furthermore, both succinate and pyruvate malate-supported H2O2 release showed significant increases only after 45 min of ischemia. Similarly, whole antioxidant capacity significantlyincreased and susceptibility to oxidants significantly decreased after 45 min of ischemia. Such changes were likely due to the accumulation of reducing equivalents, which are able to remove peroxides and maintain thiols in areduced state. This condition, which protects mitochondria against oxidants, increases mitochondrial production of oxyradicals and oxidative damage during reperfusion. This could explain the smaller functional recovery of the tissue and the farther decline of the mitochondrial function after reperfusion following the longer period of oxygen deprivation.

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Documento generato il 27/01/20 alle ore 07:16:02