Li Guo-Xiang, Tang You-Zhi, Liu Zai-Qun
Department of Organic Chemistry, College of Chemistry, Jilin University, Changchun 130021, China.
J Pharm Pharmacol. 2007 May;59(5):739-43. doi: 10.1211/jpp.59.5.0016.
Vitamin C is a popular antioxidant; however, its water solubility limits its function in the lipid environment. As a result, the antioxidative properties of its lipophilic derivatives have aroused research attention, especially L-ascorbyl-6-laurate (VC-12). We have investigated the effect of a high concentration of VC-12 on 2,2'-azobis(2-amidinopropane hydrochloride) (AAPH)-induced haemolysis of human erythrocytes. The findings indicated that VC-12 was capable of protecting erythrocytes against AAPH-induced haemolysis when its concentration was below 60 microM. With an increase in the concentration of VC-12 and a decrease in the concentration of AAPH, VC-12 promoted haemolysis remarkably, the mechanism of which has been proposed as VC-12-mediated peroxidation. When the concentration of VC-12 was increased to above 150 microM, VC-12 promoted haemolysis by its function as a surfactant, to unbalance the osmotic pressure within and outside erythrocytes. High concentrations of VC-12 may have generated radicals via autooxidation, resulting in eventual haemolysis. Therefore, the double-faced effect of VC-12 on haemolysis of human erythrocytes was due to its concentration. This information may be useful for the safe use of lipophilic vitamin C.
维生素C是一种广为人知的抗氧化剂；然而，其水溶性限制了它在脂质环境中的功能。因此，其亲脂性衍生物的抗氧化特性引起了研究关注，尤其是L-抗坏血酸-6-月桂酸酯（VC-12）。我们研究了高浓度的VC-12对2,2'-偶氮二异丁脒盐酸盐（AAPH）诱导的人红细胞溶血的影响。研究结果表明，当VC-12浓度低于60微摩尔时，它能够保护红细胞免受AAPH诱导的溶血。随着VC-12浓度的增加和AAPH浓度的降低，VC-12显著促进溶血，其机制被认为是VC-12介导的过氧化作用。当VC-12浓度增加到150微摩尔以上时，VC-12作为表面活性剂发挥作用，破坏红细胞内外的渗透压平衡，从而促进溶血。高浓度的VC-12可能通过自氧化产生自由基，最终导致溶血。因此，VC-12对人红细胞溶血的双面作用取决于其浓度。这些信息可能有助于亲脂性维生素C的安全使用。
