Pyridoxine and pyridoxamine inhibits
superoxide radicals and prevents lipid peroxidation, protein
glycosylation, and (Na+ + K+)-ATPase activity reduction in high
glucose-treated human erythrocytes.
Jain SK, Lim G.
Department of Pediatrics
Louisiana State University Health Sciences Center
1501 Kings Highway, Shreveport, LA, 71130
sjain@lsuhsc.edu
Free Radic Biol Med. 2001 Feb 1;30(3):232-7.
Abstract
Vitamin B(6) (pyridoxine)
supplementation has been found beneficial in preventing diabetic
neuropathy and retinopathy, and the glycosylation of proteins. Oxygen
radicals and oxidative damage have been implicated in the cellular
dysfunction and complications of diabetes. This study was undertaken to
test the hypothesis that pyridoxine (P) and pyridoxamine inhibit
superoxide radical production, reduce lipid peroxidation and
glycosylation, and increase the (Na+ + K+)-ATPase activity in high
glucose-exposed red blood cells (RBC). Superoxide radical production was
assessed by the reduction of cytochrome C by glucose in the presence and
absence of P or pyridoxamine in a cell-free buffered solution. To
examine cellular effects, washed normal human RBC were treated with
control and high glucose concentrations with and without P or
pyridoxamine. Both P and pyridoxamine significantly lowered lipid
peroxidation and glycated hemoglobin (HbA(1)) formation in high
glucose-exposed RBC. P and pyridoxamine significantly prevented the
reduction in (Na+ + K+)-ATPase activity in high glucose-treated RBC.
Thus, P or pyridoxamine can inhibit oxygen radical production, which in
turn prevents the lipid peroxidation, protein glycosylation, and (Na+ +
K+)-ATPase activity reduction induced by the hyperglycemia. This study
describes a new biochemical mechanism by which P or pyridoxamine
supplementation may delay or inhibit the development of complications in
diabetes.
