Ej. Lesnefsky et al., Aging decreases electron transport complex III activity in heart interfibrillar mitochondria by alteration of the cytochrome c binding site, J MOL CEL C, 33(1), 2001, pp. 37-47
Aging alters cardiac physiology and structure and enhances damage during is
chemia and reperfusion. Aging selectively decreases the rate of oxidative p
hosphorylation in the interfibrillar population of cardiac mitochondria (IF
M) located among the myofibers, whereas subsarcolemmal mitochondria (SSM) l
ocated beneath the plasma membrane remain unaffected, Aging decreased the r
ate of oxidative phosphorylation using durohydroquinone, an electron donor
to complex III, in IFM only, Complex III activity was decreased in IFM, but
not SSM, Aging did not alter the content of catalytic centers of complex I
II (cytochromes b and c, and iron-sulfur protein), Complex III activity mea
sured at physiologic ionic strength in IFM from aging hearts was decreased
by 49% compared to IFM from adults, whereas activity measured at low ionic
strength was unchanged, localizing the aging defect to the cytochrome c bin
ding site of complex III, Subunits VIII and X of the cytochrome c binding s
ite were present in complex III with the aging defect, indicating that loss
of subunits did not occur, Study of aging damage to complex III will help
clarify the contribution of altered electron transport in IFM to increased
oxidant production during aging, formation of the aging cardiac phenotype,
and the relationship of aging defects to increased damage following ischemi
a, (C) 2000 Academic Press.