Aluminum salts stimulate luminol-enhanced chemiluminescence production by human neutrophils

• Published in: Free radical research communications Vol. 14; no. 1; p. 47
• Main Authors: Stankovic, A, Mitrovic, D R
• Format: Journal Article
• Language: English
• Published: Switzerland 1991
• Subjects: Alum Compounds - pharmacology; Aluminum - pharmacology; Aluminum Compounds; Azides - pharmacology; Chlorides - pharmacology; Cytochalasin B - pharmacology; Deferoxamine - pharmacology; Edetic Acid - pharmacology; Ferric Compounds - pharmacology; Humans; Luminescent Measurements; Luminol - pharmacology; Neutrophils - drug effects; Neutrophils - physiology; Pentetic Acid - pharmacology; Sodium Azide
• ISSN: 8755-0199
• DOI: 10.3109/10715769109088941

Aluminum intoxication is currently thought to play a major role in the development of Alzheimer's disease and in certain pathologic manifestations seen during long-term hemodialysis and aging. The hypothesis that aluminum toxicity is mediated via an increased free radical production was tested by studying the effects of two aluminum and five other metallic compounds on the production of luminol-enhanced chemiluminescence (LECL) by human neutrophils. AlCl3, Al2(SO4)3 and FeCl3 were found to stimulate LECL production by human neutrophils whereas FeCl2, CuCl, CuCl2, AuCl3 were inactive. Metal chelators such as Desferal, EDTA and DETAPA suppressed aluminum-induced stimulation and depressed cell-dependent LECL below basal levels. Sodium azide and Cytochalasin B greatly depressed both basal and aluminum-induced stimulation of LECL production, suggesting that, in this system, most of this stimulation was due to myeloperoxidase. These results suggest that high tissue aluminum concentrations may induce cell-tissue lesions by stimulating local production or release of mediators of tissue damage.