Liu J, Mori A, Ogata K
Department of Neuroscience, Okayama University Medical School, Japan.
Res Commun Chem Pathol Pharmacol. 1993 Nov;82(2):151-66.
L-Ascorbic acid 2-(20 beta-11-oxo-olean-12-en-29-oic acid ethylester-3-beta-yl hydrogen phosphate) sodium salt (GEPC) is a newly synthesized compound representing a phosphate diester linkage of glycyrrhetic acid ethylester and ascorbic acid. In the present study, we found that GEPC effectively inhibited Fe(III)-ADP/NADPH-induced peroxidation of liver microsomes. The inhibitory effect was much greater than that of glycyrrhetic acid (GA), and contrasted with the stimulatory effect of ascorbic acid. An ESR study showed that GEPC appeared to have a great loss of the DPPH and superoxide radical scavenging effects of ascorbic acid. However, GEPC, like ascorbic acid, inhibited hydroxyl radicals generation in both Fe(II)-H2 O2 and Cr(VI)-H2 O2 systems. GEPC, unlike ascorbic acid, showed no pro-oxidant effect and acted as an effective iron-chelating agent in the ESR study or in the iron-induced deoxyribose and DNA degradation assays. The hydroxyl radical scavenging effect of GEPC was further demonstrated by its protective effect on the hydroxyl radical- induced degradation of certain biomolecules, i.e., carbohydrates, amino acids, and DNA. These results demonstrate that beside its protective effect on ascorbic acid autoxidation and increasing water solubility of GA, GEPC is also an antioxidant though not so powerful as ascorbic acid but more powerful than GA.
L-抗坏血酸2-(20β-11-氧代-齐墩果-12-烯-29-酸乙酯-3-β-基磷酸氢)钠盐（GEPC）是一种新合成的化合物，它代表甘草次酸乙酯与抗坏血酸之间的磷酸二酯键。在本研究中，我们发现GEPC能有效抑制Fe(III)-ADP/NADPH诱导的肝微粒体过氧化反应。其抑制作用远大于甘草次酸（GA），且与抗坏血酸的刺激作用形成对比。电子自旋共振（ESR）研究表明，GEPC似乎大量丧失了抗坏血酸的二苯基苦味酰基自由基（DPPH）和超氧阴离子自由基清除作用。然而，与抗坏血酸一样，GEPC在Fe(II)-H₂O₂和Cr(VI)-H₂O₂体系中均能抑制羟基自由基的产生。与抗坏血酸不同，在ESR研究或铁诱导的脱氧核糖和DNA降解试验中，GEPC未表现出促氧化作用，而是作为一种有效的铁螯合剂。GEPC对某些生物分子（即碳水化合物、氨基酸和DNA）羟基自由基诱导降解的保护作用进一步证明了其羟基自由基清除作用。这些结果表明，除了对抗坏血酸自氧化有保护作用以及增加GA的水溶性外，GEPC也是一种抗氧化剂，虽然不如抗坏血酸强大，但比GA更强大。
