Aluminum compounds enhance lipid peroxidation in liposomes: Insight into cellular damage caused by oxidative stress

Aluminum (Al) has been proposed as one of the critical environmental factors responsible for several neurodegenerative diseases such as Alzheimer’s disease. However, the suggested mechanism involving the contribution of reactive oxygen species still remains controversial. We have first attempted to identify Al compounds either in its ionic or complexed forms that cause oxidative stress in biological systems. For this purpose, we examined the effect of inorganic Fe2+- and organic radical initiator (2,2′-azobis (2-amidinopopane) hydrochloride; AAPH)-induced lipid peroxidation by using aluminum (Al3+) nitrate and tris(maltolato)aluminum(III) complex (ALM) with respect to molecular oxygen (O2) consumption and membrane fluidity change in liposomes as biological membrane models. The following important results were obtained: (1) ALM enhanced the lipid peroxidation induced by Fe2+ and AAPH in phosphatidylcholine liposomes; this corresponded well with the promotion of O2 uptake in the same liposomes, (2) Al3+ increased both lipid peroxidation and O2 consumption in phosphatidylserine liposomes in the presence of Fe2+, and (3) both Al3+ and ALM affected the membrane fluidity on the inner side. It has been concluded that ALM induces higher lipid peroxidation in liposomes than Al3+; this finding will be useful to gain an insight into the role of Al in cellular damage in relation to oxidative stress.