The Neurotoxicity Induced By Acetaldehyde And The Protective Effects Of Astaxanthin

In this study, human neuroblastoma SH-SY5Y cell line is used as a model tostudy the neurotoxic effects of acetaldehyde, a major ethanol metabolite in the body,and the protective effects of antioxidant astaxanthin on acetaldehyde-induced celltoxicity.It is found that acetaldehyde decrease the cell survival and induce the activity ofcaspase-3in a dose-dependent manner. The expression of anti-apoptotic proteinsBcl-2and Bcl-xl is decreased while the expression of pro-apoptotic proteins Bax isincreased by acetaldehyde treatments. The levels of MDA, an indicator of oxidativestress, are also raised by acetaldehyde treatments. Pretreatment with astaxanthininhibit acetaldehyde-induced caspase-3activity and downregulation of Bcl-2/Baxand Bcl-xl/Bax expression, and improve the cell survival. Astaxanthin pretreatmentalso inhibit the increase of MDA induced by acetaldehyde.The conclusion is that acetaldehyde may inhibit SH-SY5Y cell survival andinduce apoptosis by induction of intracellular oxidative stress, and bydownregulation of anti-apoptotic protein Bcl-2and Bcl-xl and upregulation ofproapototic proteins Bax. And astaxanthin may improve SH-SY5Y cell survival andinhibit cell apoptosis through regulating the expression of above bcl-2familyproteins and inhibiting the oxidative stress induced by acetaldehyde.