Flavonoids from grape seeds prevent increased alcohol-induced neuronal lipofuscin formation

In a previous study, we found that prolonged oxidative stress produced by chronic ethanol consumption leads to an increased formation of lipofuscin in hippocampal and cerebellar neurons. This pigment is an end-result of lipid peroxidation. Flavanols, which abound in the human diet, are known to exert a powerful in-vitro antioxidant action. Therefore, to evaluate whether these compounds might display beneficial effects in the rat brain, we examined whether or not these natural antioxidants would impede neuronal ethanol-induced lipofuscin accumulation.

Adult rats were fed for 6 months either with 20% ethanol solution or with the same solution to which a mixture of grape seed catechins and oligomeric procyanidins (200 mg/l) was added. Controls ingested either tap water or water supplemented with the antioxidant compound. The total amount of lipofuscin in the hippocampal CA1 and CA3 pyramids and in the cerebellar Purkinje cells was estimated by applying unbiased stereological methods. The mean volume of the neurons was estimated using the nucleator and the volumetric density of lipofuscin was calculated by point counting.

Flavanols prevented the accumulation of neuronal lipofuscin in the animals submitted to ethanol feeding (i.e. under conditions of increased oxidative stress) but not in the water-drinking controls. The neuronal volume did not alter among the groups studied.

Data obtained show that consumption of flavanols can reduce the effects of oxidative activity brought about by alcohol consumption, indicating that these compounds might display neuronal beneficial effects under oxidative stress.