Paul V N, Chopra K, Kulkarni S K
Pharmacology Division, University Institute of Pharmaceutical Sciences, Panjab University, Chandigarh, India.
Methods Find Exp Clin Pharmacol. 2000 Sep;22(7):551-5.
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.
本研究旨在探讨组氨酸对缺氧应激啮齿动物模型以及对小鼠脑匀浆中三价铁离子-抗坏血酸诱导的脂质过氧化反应中活性氧的影响。在组氨酸处理的动物中，缺氧应激诱导惊厥发作的潜伏期缩短，同时脑脂质过氧化水平升高。在体外，组氨酸增强了小鼠脑匀浆中三价铁离子-抗坏血酸诱导的脂质过氧化反应，而其他抗氧化剂如丁基羟基甲苯（B-HT）和U-74500A则抑制了该反应。此外，高浓度抗坏血酸预孵育系统并不能抑制三价铁离子-组氨酸诱导的脂质过氧化反应。因此，得出结论：组氨酸作为一种强促氧化剂，在缺氧应激以及三价铁离子-抗坏血酸诱导的脂质过氧化反应过程中增强活性氧的生成。
