Abstract
An attempt was made to study the effect of histidine on reactive oxygen species in a rodent model of hypoxic stress and in Fe(3+)-ascorbic acid-induced lipid peroxidation in mouse brain homogenates. The latency for onset of hypoxic stress-induced convulsions was decreased in histidine-treated animals with a concomitant rise in brain lipid peroxidation levels. In vitro, histidine potentiated Fe(3+)-ascorbic acid-induced lipid peroxidation in mouse brain homogenates while other antioxidants like B-HT and U-74500A inhibited the same. Moreover, Fe(3+)-histidine-induced lipid peroxidation could not be inhibited by preincubation of the system with high concentrations of ascorbic acid. Thus, it is concluded that histidine acts as a strong prooxidant potentiating the genesis of reactive oxygen species during hypoxic stress as well as during Fe(3+)-ascorbic acid-induced lipid peroxidation.
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