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目的：探讨葡萄糖－６－磷酸脱氢酶（Ｇ６ＰＤ）缺乏症溶血的生化机制。方法：采用荧光偏振法测定红细胞膜脂流动性；荧光分光光度法测定膜过氧化脂质（ＭＤＡ）；硅胶柱层析及薄板层析分离磷脂，气相色谱法分析磷脂中脂肪酸含量。结果：Ｇ６ＰＤ缺乏症荧光偏振度为０．２６３３±０．００４３，较正常对照的０．２２６１±０．００６９高（Ｐ＜０．０１）；Ｇ６ＰＤ缺乏时ＭＤＡ含量为１．４８２±０．０９５ｎｍｏｌ／ｍｇ膜蛋白，正常对照为０．３８２±０．０７２ｎｍｏｌ／ｍｇ膜蛋白（Ｐ＜０．０１）；Ｇ６ＰＤ缺乏症总磷脂及磷脂酰丝氨酸中不饱和脂肪酸Ｃ１８∶１，Ｃ１８∶２含量减少（Ｐ均＜０．０５）。结论：红细胞膜脂流动性降低可能是Ｇ６ＰＤ缺乏症溶血的一个重要原因。
Objective: To investigate the biochemical mechanism of hemolysis of glucose-6-phosphate dehydrogenase (G6PD) deficiency. Methods: Fluorescence polarization was used to determine the membrane fluidity of erythrocytes. The membrane lipid peroxidation (MDA) was determined by fluorescence spectrophotometry. The phospholipids were separated by silica gel column chromatography and thin layer chromatography. The content of fatty acids in phospholipids was analyzed by gas chromatography. Results: The fluorescence polarization degree of G6PD deficiency was 0.2633 ± 0.0043, which was higher than that of the normal control (0.2261 ± 0.0069) (P <0.01). The MDA content of G6PD deficiency was 1.482 ± 0.095 nmol / Mg membrane protein, the normal control was 0.382 ± 0.072nmol / mg membrane protein (P <0.01); The content of unsaturated fatty acids C18:1, C18:2 in G6PD deficiency total lipids and phosphatidylserine decreased P <0.05). Conclusion: The decrease of erythrocyte membrane fluidity may be an important reason for the hemolysis of G6PD deficiency.