Muscoli C, Fresta M, Cardile V, Palumbo M, Renis M,
Puglisi G, Paolino D, Nistico S, Rotiroti D, Mollace V.
Department of Pharmacobiological Sciences,
University of Catanzaro Magna Graecia,
Complesso Nini Barbieri,
I-88021 Roccelletta di Borgia, Catanzaro, Italy.
Neurosci Lett 2002 Aug 23;329(1):21-4
Ethanol-induced neurological disorders have recently been characterised. Indeed, evidence has been collected indicating that chronic ethanol consumption leads to direct or indirect changes in the viability of central nervous system cells. Here we investigated the role of free radical overproduction in primary cortical rat astroglial cells undergoing chronic treatment with ethanol (100 microM). In particular, exposure of astroglial cell cultures to ethanol for 12 consecutive days produced an increased release of lactic dehydrogenase, a decrease on glutamine synthase activity being both effects accompanied by decrease in astroglial viability as detected by MTT (Thiazolyl Blue) test. These effects were accompanied by an increased formation of malondialdehyde (a marker of lipid peroxidation) and by abnormal formation of heat shock protein, being both effects antagonised by liposomally entrapped
idebenone, a non-peptidyl free radical scavenger. Taken together, these results suggest that ethanol-induced injury on astroglial cells are mediated by abnormal formation of free radical species and this may represent a useful approach in the treatment of ethanol-related brain disorders.