Effect of non-enzymatic glycation on aluminium-induced lipid peroxidation of human high density lipoproteins (HDL)

Background and Aim: Several studies have shown that non-enzymatic glycation and oxidative damage play an important role in the pathogenesis of neurological diseases. Increased levels of advanced glycation end-products (AGEs) and of lipid peroxidation products have been observed in the brain, in the cerebrospinal fluid (CSF) and in the plasma of subjects affected by Alzheimer's disease (AD). The aim of this study was to investigate the effect of non-enzymatic glycation on aluminium-induced lipid peroxidation and on the stimulatory effect exerted by aluminium on iron-triggered oxidation of high density lipoproteins (HDL) isolated from human plasma. Methods and Results: Aluminium (10-200 muM) and iron (20 muM) induced a significant increase in lipid hydroperoxides in HDL compared to untreated HDL. Therefore, our results confirm that aluminum and iron exert an oxidant effect on HDL. Moreover, aluminium exerted a stimulatory effect on iron-induced lipid peroxidation of HDL, in agreement with our previous studies. The aluminum/iron-induced increase in lipid hydroperoxides was significantly higher in HDL incubated for different time periods (24-72 hours) in the presence of 50 mM glucose (Gly-HDL) compared to HDL incubated alone. These results demonstrate that Gly-HDL is more susceptible to aluminium and iron-oxidative treatment with respect to control HDL. Conclusion: We suggest that aluminium and iron-induced oxidative damage on HDL could be involved in the development of neurological diseases and that glycation of HDL could represent an additional risk factor for these human diseases. (C) 2004, Medikal Press.