An attempt was made to study the effect of histidine on reactive oxygen spe
cies in a rodent model of hypoxic stress and in Fe3+-ascorbic acid induced
lipid peroxidation in mouse brain homogenates. The latency for onset of hyp
oxic stress-induced convulsions was decreased in histidine-treated animals
with a concomitant rise in brain lipid peroxidation levels. In vitro, histi
dine potentiated Fe3+-ascorbic acid-indirected lipid peroxidation irt mouse
brain homogenates while other antioxidants like B-HT and U-74500A inhibite
d the same. Moreover; Fe3+-histidine-induced lipid peroxidation could nor b
e inhibited by preincubation for the system with high concentrations of asc
orbic acid. Thus, it is concluded that histidine nets as a strong prooxidan
t potentiating the genesis of reactive oxygen species during hypoxic stress
as well as during Fe3+-ascorbic acid-induced lipid peroxidation. (C) 2000
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