Yoshikawa T, Naito Y, Tanigawa T, Yoneta T, Kondo M
First Department of Medicine, Kyoto Prefectural University of Medicine, Japan.
Biochim Biophys Acta. 1991 Nov 14;1115(1):15-22. doi: 10.1016/0304-4165(91)90005-2.
A zinc-carnosine chelate compound, Z-103, attenuates gastric mucosal injuries and inhibits the increase of lipid peroxide in the gastric mucosa induced by burn shock or ischemia-reperfusion. However, the exact mechanism of the antioxidative effect of Z-103 is not clear. The antioxidant properties of a novel anti-peptic ulcer agent Z-103 in vitro were compared with those of zinc ion and L-carnosine. Z-103 scavenged superoxide anion radicals. Z-103 and ZnSO4, but not L-carnosine, inhibited the superoxide generation from polymorphonuclear leukocytes stimulated by opsonized zymosan, and also inhibited the generation of hydroxyl radicals by the Fenton reaction. The increase of lipid peroxides produced by rat brain homogenates and liver microsomes was also inhibited by Z-103 and ZnSO4. These findings indicate that the strong anti-ulcer and antioxidative actions of Z-103 in vivo are due to a combination of these antioxidant actions in vitro.
一种锌 - 肌肽螯合物化合物Z - 103可减轻胃黏膜损伤,并抑制由烧伤休克或缺血再灌注引起的胃黏膜中脂质过氧化物的增加。然而,Z - 103抗氧化作用的确切机制尚不清楚。将新型抗消化性溃疡药物Z - 103的体外抗氧化特性与锌离子和L - 肌肽的抗氧化特性进行了比较。Z - 103清除超氧阴离子自由基。Z - 103和硫酸锌(ZnSO4)而非L - 肌肽,抑制了经调理酵母聚糖刺激的多形核白细胞产生超氧化物,并且也抑制了芬顿反应产生的羟基自由基。Z - 103和硫酸锌(ZnSO4)还抑制了大鼠脑匀浆和肝微粒体产生的脂质过氧化物的增加。这些发现表明,Z - 103在体内的强大抗溃疡和抗氧化作用是由于其体外这些抗氧化作用的综合结果。