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
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.