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Membrane Transport Group, Department of Chemistry, The Faculties, The Australian National University, Canberra, Australian Capital Territory 0200, Australia
The use of
electrophysiological and molecular biology techniques has shed light on
reactive oxygen species (ROS)-induced impairment of surface and
internal membranes that control cellular signaling. These deleterious
effects of ROS are due to their interaction with various ion transport
proteins underlying the transmembrane signal transduction, namely,
1) ion channels, such as
Ca2+ channels (including
voltage-sensitive L-type Ca2+
currents, dihydropyridine receptor voltage sensors, ryanodine receptor
Ca2+-release channels, and
D-myo-inositol
1,4,5-trisphosphate receptor Ca2+-release channels),
K+ channels (such as
Ca2+-activated
K+ channels, inward and outward
K+ currents, and ATP-sensitive
K+ channels),
Na+ channels, and
Cl
channels;
2) ion pumps, such as sarcoplasmic
reticulum and sarcolemmal Ca2+
pumps,
Na+-K+-ATPase
(Na+ pump), and
H+-ATPase
(H+ pump);
3) ion exchangers such as the
Na+/Ca2+
exchanger and
Na+/H+
exchanger; and 4) ion cotransporters
such as
K+-Cl,
Na+-K+-Cl,
and
Pi-Na+
cotransporters. The mechanism of ROS-induced modifications
in ion transport pathways involves
1) oxidation of sulfhydryl groups located on the ion transport proteins,
2) peroxidation of membrane phospholipids, and 3) inhibition of
membrane-bound regulatory enzymes and modification of the oxidative
phosphorylation and ATP levels. Alterations in the ion transport
mechanisms lead to changes in a second messenger system, primarily
Ca2+ homeostasis, which further
augment the abnormal electrical activity and distortion of signal
transduction, causing cell dysfunction, which underlies pathological
conditions.
ischemia-reperfusion; muscle pathologies; thiol group; calcium homeostasis; membrane compartmentation; reducing and oxidizing agents
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