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Titolo:
Surviving hypoxia without really dying
Autore:
Boutilier, RG; St-Pierre, J;
Indirizzi:
Univ Cambridge, Dept Zool, Cambridge CB2 3EJ, England Univ Cambridge Cambridge England CB2 3EJ ool, Cambridge CB2 3EJ, England
Titolo Testata:
COMPARATIVE BIOCHEMISTRY AND PHYSIOLOGY A-MOLECULAR AND INTEGRATIVE PHYSIOLOGY
fascicolo: 4, volume: 126, anno: 2000,
pagine: 481 - 490
SICI:
1095-6433(200008)126:4<481:SHWRD>2.0.ZU;2-N
Fonte:
ISI
Lingua:
ENG
Soggetto:
HEART-RATE HEARTS; ANOXIA-TOLERANT HEPATOCYTES; METABOLIC-RATE; TURTLE BRAIN; ADENOSINE 5'-TRIPHOSPHATASE; CARDIAC-MUSCLE; MODEL SYSTEM; K+ CHANNELS; SLOW; ISCHEMIA;
Keywords:
anoxia; hypoxia; ion channels; ATP turnover; metabolism; membranes; mitochondria;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Agriculture,Biology & Environmental Sciences
Life Sciences
Citazioni:
45
Recensione:
Indirizzi per estratti:
Indirizzo: Boutilier, RG Univ Cambridge, Dept Zool, Downing St, Cambridge CB2 3EJ, England Univ Cambridge Downing St Cambridge England CB2 3EJ England
Citazione:
R.G. Boutilier e J. St-Pierre, "Surviving hypoxia without really dying", COMP BIOC A, 126(4), 2000, pp. 481-490

Abstract

In cases of severe O-2 limitation, most excitable cells of mammals cannot continue to meet the energy demands of active ion transporting systems, leading to catastrophic membrane failure and cell death. However, in certain lower vertebrates, hypoxia-induced membrane destabilisation of the kind seenin mammals is either slow to develop or does not occur at all owing to adaptive decreases in membrane permeability (i.e. ion 'channel arrest'), that dramatically reduce the energetic costs of ion-balancing ATPases. Mammaliancells do, however, exhibit a whole host of adaptive responses to less severe shortages of oxygen, which include energy-balanced metabolic suppression, ionic-induced activation of O-2 receptors and the upregulation of certaingenes,all of which enhance the systemic delivery of oxygen and promote energy conservation. Accumulating evidence suggests that the mechanisms underlying these protective effects are orchestrated into action by putative members of an O-2-sensing pathway that most if not all cells share in common. In this review we address three major questions: (i) how do cells detect shortages of oxygen and subsequently set in motion adaptive mechanisms of either energy production or energy conservation; (ii) how do these mechanisms restructure cellular pathways of ATP supply and demand to ensure that ion-motive: ATPases are given priority over other cell functions to preserve membrane integrity in energy-limited states; and (iii) what mechanisms of molecular and metabolic defence against acute and long-term shortages of oxygen set hypoxia-tolerant systems apart from their hypoxia-sensitive counterparts? (C) 2000 Elsevier Science Inc. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 11/07/20 alle ore 03:00:56