Sakuma S, Fujimoto Y, Nishida H, Sumiya T, Yamamoto I, Fujita T
Department of Hygienic Chemistry, Osaka University of Pharmaceutical Sciences, Japan.
Prostaglandins. 1992 May;43(5):435-43. doi: 10.1016/0090-6980(92)90126-e.
t-Butyl hydroperoxide and H2O2-Fe(2+)-EDTA-glutathione system which produces hydroxyl radicals did not affect the 15-hydroxy prostaglandin dehydrogenase activity in rabbit kidney cortex. On the other hand, H2O2-Fe(2+)-EDTA-glutathione system inhibited the prostaglandin delta 13 reductase activity. Mannitol, a scavenger of hydroxyl radicals, had no effect on the inhibitory action of this system, indicating that the effect of H2O2-Fe(2+)-EDTA-glutathione system on the prostaglandin delta 13 reductase may not be due to produced hydroxyl radicals. As a result of further investigation, it was shown that glutathione disulfide, which is synthesized concomitantly with hydroxyl radicals from H2O2-Fe(2+)-EDTA-glutathione, inhibited the prostaglandin delta 13 reductase activity. These results suggest that hydroperoxides and hydroxyl radicals may not be likely candidates for the modulator of the catabolism of prostaglandins in the kidney cortex, and that glutathione disulfide has the potential to modulate the prostaglandin catabolism by affecting the prostaglandin delta 13 reductase activity.
叔丁基过氧化氢以及能产生羟基自由基的H2O2 - Fe(2+) - EDTA - 谷胱甘肽体系并未影响兔肾皮质中15 - 羟基前列腺素脱氢酶的活性。另一方面，H2O2 - Fe(2+) - EDTA - 谷胱甘肽体系抑制了前列腺素δ13还原酶的活性。羟基自由基清除剂甘露醇对该体系的抑制作用没有影响，这表明H2O2 - Fe(2+) - EDTA - 谷胱甘肽体系对前列腺素δ13还原酶的作用可能并非由产生的羟基自由基所致。进一步研究结果表明，与H2O2 - Fe(2+) - EDTA - 谷胱甘肽产生的羟基自由基同时合成的谷胱甘肽二硫化物抑制了前列腺素δ13还原酶的活性。这些结果提示，氢过氧化物和羟基自由基可能不太可能是肾皮质中前列腺素分解代谢调节因子的候选物质，而谷胱甘肽二硫化物有可能通过影响前列腺素δ13还原酶的活性来调节前列腺素的分解代谢。
