HUMAN EPIDERMAL-CELLS PROGRESSIVELY LOSE THEIR CARDIOLIPINS DURING AGING WITHOUT CHANGE IN MITOCHONDRIAL TRANSMEMBRANE POTENTIAL

Citation
A. Maftah et al., HUMAN EPIDERMAL-CELLS PROGRESSIVELY LOSE THEIR CARDIOLIPINS DURING AGING WITHOUT CHANGE IN MITOCHONDRIAL TRANSMEMBRANE POTENTIAL, Mechanism of ageing and development, 77(2), 1994, pp. 83-96
Citations number
70
Categorie Soggetti
Geiatric & Gerontology
ISSN journal
00476374
Volume
77
Issue
2
Year of publication
1994
Pages
83 - 96
Database
ISI
SICI code
0047-6374(1994)77:2<83:HEPLTC>2.0.ZU;2-R
Abstract
Mitochondria dysfunction is considered to be a major cause of the modi fications that occur during cell ageing. For this reason, cardiolipin, a suitable marker of the chondriome, as well as the mitochondrial tra nsmembrane potential were examined in keratinocytes obtained from 9- t o 75-year-oId women. The study was carried out by flow cytometry using two fluorescent mitochondria probes: nonyl acridine orange, which bin ds specifically to cardiolipin, and rhodamine 123, which is incorporat ed mainly in response to transmembrane potential. Cardiolipin levels i n cells from elderly donors (75 years old) would be 57% lower (r = 0.5 40; P = 0.0002) than those in children (9 years old), while the inner transmembrane potential remained unchanged (r = 0.0394; P = 0.8017). T he stability of the membrane potential may be explained by either or b oth of the following hypotheses: (i) the same pool of organelles able to maintain membrane potential is conserved even when cardiolipin leve ls decrease (ii) mitochondria membrane potential does indeed decrease with age but is compensated by glycolysis energy production. Finally, it may be stated that the fluorescent probes nonyl acridine orange and rhodamine 123 might be of interest in testing the phenotype of senesc ent cells and would be useful in screening the role of certain specifi c genes in cell ageing.