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The operation of Na+/Ca2+ exchanger prevents intracellular Ca2+ overload and hepatocyte killing following iron-induced lipid peroxidation.

Abstract：

:Stimulation of lipid peroxidation by incubating isolated rat hepatocytes with ADP/FeCl3 caused a time dependent increase in cytosolic free Ca2+ levels, without influencing cellular Na+ content. Omission of Na+ from the incubation medium greatly increased the accumulation of Ca2+, which was partially reverted upon transferring the cells in a Na+ containing medium. This suggested that a Na(+)-dependent Ca2+ transporter was activated upon the elevation of cytosolic Ca2+ and partially counteracted the influx of Ca2+ promoted by lipid peroxidation. In the presence of Na+ cell death was not associated with the increase of Ca2+ induced by peroxidative injury; however, decrease of mitochondrial membrane potential and loss of cell viability followed by massive accumulation of Ca2+ occurring in hepatocytes incubated with ADP/FeCl3 in a Na(+)-free medium. Both these effects were completely prevented by chelation of extracellular Ca2+ with EGTA. Thus, we conclude that Na(+)-dependent Ca2+ transporter is involved in controlling excessive accumulation of Ca2+ induced by stimulation of lipid peroxidation and can prevent hepatocyte death caused by Ca(2+)-dependent alterations of mitochondrial activity.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Carini R,Bellomo G,Dianzani MU,Albano E

doi

10.1006/bbrc.1995.1409

subject

Has Abstract

pub_date

1995-03-17 00:00:00

pages

813-8

issue

2

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(85)71409-X

journal_volume

208

pub_type

杂志文章

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