ULTRACYTOCHEMICAL STUDIES OF THE EFFECTS OF ALUMINUM ON THE BLOOD-BRAIN-BARRIER OF MICE

We studied the effect of chronic exposure (6 weeks and 6 months) of mi ce to drinking (tap) water containing 1.76% (0.06 M) aluminum lactate on some cytochemical properties of the blood-brain barrier (BBB). The plasmalemma-bound enzymatic activities of alkaline phosphatase (AP) an d Ca2+-activated adenosine triphosphatase (Ca2+-ATPase) were studied a t the ultrastructural level. Anionic sites were localized with cationi zed ferritin in a pre-embedding procedure and with cationic colloidal gold in a post-embedding procedure applied to brain samples embedded i n Lowicryl K4M. Intravenously injected Evans blue and horseradish pero xidase (HRP) were used for evaluation of the functional state of the B BB. The results indicate that chronic exposure to aluminum does not no ticeably affect barrier function of the endothelium of cerebral cortex blood microvessels. Focal leakage of larger than capillary microvesse ls (presumably arterioles and venules) was observed only in a few area s, such as the basal ganglia and amygdaloid nuclei. The localization o f both enzymatic activities (AP and Ca2+-ATPase) in microvessels remai ned essentially unchanged. The localization of anionic sites was also unchanged except on the luminal surface of the endothelium of a few bl ood microvessels located in areas of the brain where leakage of the in jected HRP was noted. In these vessels the injected HRP was often atta ched to the luminal surface of the endothelial cells, suggesting its i ncreased stickiness. These data, compared with our previous observatio ns on brain microvascular endothelial cells growing in vitro, indicate that cytotoxicity of aluminum is evidently less pronounced in the liv ing organism, presumably due to action of detoxicating and regulatory mechanisms.