Chronic Ethanol Consumption and Thiamine Deficiency Modulate β-Amyloid Peptide Level and Oxidative Stress in the Brain

Aims: The effects of chronic ethanol (EtOH) consumption, associated or not with thiamine deficiency (TD), on beta-amyloid peptide (A beta) level and oxidative stress in the brain were studied in male C57BL/6 mice. Methods: Mice were prepared by feeding with an EtOH liquid diet, thiamine-depleted liquid diet and a thiamine-depleted EtOH liquid diet for 7 weeks. Biochemical parameters were measured by corresponding commercial kits. Results: EtOH consumption or TD induced a significant decrease in the thiamine level, but induced increased in the beta-amyloid peptide 1-42 and beta-amyloid peptide 1-40 (A beta(1-40)) levels. EtOH consumption led to a significant increase in the malondialdehyde (MDA) and nitric oxide (NO) levels, total nitric oxide synthase (NOS) activities and inducible nitric oxide synthase (iNOS) activities, but a significant decrease in superoxide dismutase (SOD) and glutathione peroxidase activities. TD significantly elevated the MDA content and total NOS and iNOS activities but lowered SOD activity. A beta(1-40) overproduction, the change in the NO level, and SOD activity in the brain induced by chronic EtOH treatment associated with TD were greater than that induced by EtOH or TD alone. Conclusion: Findings from this report suggested that chronic EtOH consumption could induce TD, excess A beta production and oxidative damage, and the association with TD should have more severe effects on the brain. Short summary: Chronic EtOH consumption or thiamine deficiency (TD) treatment could reduce the thiamine level, induce beta-amyloid peptide (A beta) overproduction and oxidative stress in the brain. When associated with TD, EtOH consumption caused A beta overproduction and oxidative damage more serious.