TY - JOUR
T1 - Antioxidant and pro-oxidant assay for a new drug GEPC
T2 - Detected by ESR spectrometry and by protective effects on lipid peroxidation and biomolecule degradation
AU - Liu, J.
AU - Mori, A.
AU - Ogata, K.
PY - 1993
Y1 - 1993
N2 - L-Ascorbic acid 2-(20β -11-oxo-olean-12-en-29-oic acid ethylester-3-β - 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)-H 2 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.
AB - L-Ascorbic acid 2-(20β -11-oxo-olean-12-en-29-oic acid ethylester-3-β - 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)-H 2 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.
UR - https://www.scopus.com/pages/publications/0027379384
M3 - 文章
C2 - 8303085
AN - SCOPUS:0027379384
SN - 0034-5164
VL - 82
SP - 151
EP - 166
JO - Research Communications in Chemical Pathology and Pharmacology
JF - Research Communications in Chemical Pathology and Pharmacology
IS - 2
ER -