Lipoic acid decreases lipid peroxidation and protein glycosylation and increases (Na++K+)- and Ca++-ATPase activities in high glucose-treated human erythrocytes
Sk. Jain et G. Lim, Lipoic acid decreases lipid peroxidation and protein glycosylation and increases (Na++K+)- and Ca++-ATPase activities in high glucose-treated human erythrocytes, FREE RAD B, 29(11), 2000, pp. 1122-1128
Lipoic acid supplementation has been found to be beneficial in preventing n
eurovascular abnormalities in diabetic neuropathy. Insufficient (Na+ + K+)-
ATPase activity has been suggested as a contributing factor in the developm
ent of diabetic neuropathy. This study was undertaken to test the hypothesi
s that lipoic acid reduces lipid peroxidation and glycosylation and can inc
rease the (Na+ + K+)- and Ca++-ATPase activities in high glucose-exposed re
d blood cells (RBC). Washed normal human RBC were treated with normal (6 mM
) and high glucose concentrations (45 mM) with 0-0.2 mM lipoic acid (mixtur
e of S and R sterioisomers) in a shaking water bath at 37 degreesC for 24 h
. There was a significant stimulation of glucose consumption by RBC in the
presence of lipoic acid both in normal and high glucose-treated RBC. Lipoic
acid significantly lowered the level of glycated hemoglobin (GHb) and lipi
d peroxidation in RBC exposed to high glucose concentrations. High glucose
treatment significantly lowered the activities of (Na+ + K+)- and Ca++-ATPa
ses of RBC membranes. Lipoic acid addition significantly blocked the reduct
ion in activities of (Na+ + K+)- and Ca++ -ATPases in high glucose- treated
RBC. There were no differences in lipid peroxidation, GHb and(Na+ + K+)- a
nd Ca++-ATPase activity levels in normal glucose-treated RBC with and witho
ut lipoic acid. Thus, Lipoic acid can lower lipid peroxidation and protein
glycosylation, and increase (Na+ + K+)- and Ca++-ATPase activities in high-
glucose exposed RBC, which provides a potential mechanism by which lipoic a
cid may delay or inhibit the development of neuropathy in diabetes. (C) 200
0 Elsevier Science Inc.