Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/99854
Type: Artigo de periódico
Title: Ca2+ Transport And Oxidative Damage Of Mitochondria.
Author: Vercesi A.E.
Abstract: 1. Mitochondria from a wide range of sources have the ability to accumulate Ca2+ down their electrochemical gradient mediated by a uniport mechanism. 2. Ca2+ efflux occurs via two separate pathways: a Na+/Ca2+ exchanger that predominates in mitochondria from excitable tissues and a Na(+)-independent pathway that predominates in mitochondria from non-excitable tissues. 3. The kinetic characteristics of these calcium influx-efflux pathways appear to be incompatible with any role for mitochondria as cytosolic Ca2+ buffers, under resting normal physiological conditions. Instead, the biological role of this Ca(2+)-transporting system seems to be the regulation of matrix Ca2+ in a range that permits the regulation of three intramitochondrial Ca(2+)-dependent dehydrogenases which catalyze rate-limiting reactions of the Krebs cycle. 4. Under conditions in which a high cytosolic Ca2+ concentration is sustained, the matrix Ca2+ concentration may attain levels that lead to impairment of mitochondrial functions such as inhibition of oxidative phosphorylation and increase in inner membrane permeability. 5. Accumulation of Ca2+ by mitochondria under conditions of oxidative stress induces an increase in inner membrane permeability by a mechanism that appears to be mediated by protein polymerization due to thiol cross-linking.
Editor: 
Rights: aberto
Identifier DOI: 
Address: http://www.scopus.com/inward/record.url?eid=2-s2.0-0027589496&partnerID=40&md5=db368eefb3132afffdb876b8f1552a9b
Date Issue: 1993
Appears in Collections:Unicamp - Artigos e Outros Documentos

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