硒保护离体培养人肝细胞膜流动性的机制探讨

Study on Mechanism of Membrane Fluidity Changing in Cultured Human Hepatocytes Pretreated by Selenium

原代培养人胚细胞经不同剂量硒预保护后，用四氯化碳（ＣＣｌ４）攻击，观察细胞膜流动性及培养液中谷胱甘肽过氧化物酶（Ｓｅ－ＧＳＨ－Ｐｘ）与两二醛（ＭＤＡ）比值的变化．结果；与正常对照组比较，ＣＣｌ４损伤组肝细胞膜流动性明显降低，差异有显著性意义（Ｐ＜０．００１）。与ＣＣｌ４．损伤组比较，硒保护组股流动性显著增大．同时，Ｓｅ－ＧＳＨ－Ｐｘ活性明显提高，ＭＤＡ产生量显著减少，差异均有显著性意义（Ｐ＜０．０１）。且细胞膜流动性与Ｓｅ－ＧＳＨ－Ｐｘ／ＭＤＡ比值呈显著正相关（ｒ＝＋０．９４７３，Ｐ＜０．０１）。因此，本文认为硒可以提高Ｓｅ－ＧＳＨ－Ｐｘ／ＭＤＡ比值，增强细胞抗氧化能力，维护人肝细胞膜流动性．

To tudy possible mechanism whereby selenium(Se)may affect Iiver plasma membranefluidity.primary cultured human hepatocytes were pretreated with Se(1. 156 ×10-8￣1.156×10-6 mol/L)and then exposed to carbon tetrachloride(CCl4 2. 0 ×10 -2 mol/L),thechanges of plasma membrane fluidity and the ratio of Se-GSH-Px/MDA in medium were observed. The results showed that plasma membrane fluidity decreased significantfly in hepato-cytes treated by CCl4 as compared with that in untreated hepatocytes (P<0. 01)' A significant increase in membrane fluidity. accompany by increase in Se-GSH-Px activity and decrease in MDA production.was observed in hepatocytes protected with Se related to that innon-protected control(P<0. 01).There was a positive correlation between the hepatocytesplasma membrane fluidity and the ratio of Se-GSH-Px/MDA (γ= + 0.9473. P<0.01).Weconclude from these observations that Se could increase the ratio of Se-GSH-Px/MDA, enhance hepatocyte antioxidation capability, and thus maintain the hepatocyte plasma membrane fluidity.