Effects Of Ethanol-induced Damage And Ascorbic Acid Release On Primary Cultured Cortical Neurons

Excessive drinking and alcoholism were considered alcohol abuse. The neurotoxicity induced by alcohol abuse could lead to cerebral lesion, which was associated with the production of some free radicals due to ethanol administration. In order to clarify the effects and the possible mechanism of ethanol on the neurons, both the neuron damage induced by a long-term administration of high dose ethanol and the neuromodulator release induced by an acute administration of low dose ethanol were examined in this paper.The result showed that treatment of primary cultured rat cortical neurons with ethanol (11mM-1.1M) for 24 hours led to significant decrease in cell viability. The half-death concentration of ethanol to neurons was 380mM. Co-treatment of ethanol with ascorbic acid (AA, 400μM) or resveratrol (0.01, 0.1, 1.0, 10μg/mL) significantly protected neurons from the damage induced by ethanol (11mM or 22mM). Similarly, Pseudoginsenoside-F₁₁ (PF11, 1,10μg/mL) also inhibited the ethanol-induced damage. Moreover, polyphenols (10μg/mL) and proanthocyanidins (10μg/mL) significantly protected cells against high concentration (44mM, 110mM) ethanol-induced damage. These results indicated that all the antioxidants used in the study could eliminate the ethanol-induced damage on neurons suggesting that ethanol-induced neuronal damage was highly related to the level of free radicals.We found that ethanol could increase AA release from primary cultured neurons, the maximal increase was 200% over the normal state. The contents of grape seeds, resveratrol and proanthocyanidins could inhibit ethanol-induced AA release, while polyphenols could increase AA release. PF11 had no significant effects on ethanol-induced AA release. Furthermore, glutamate, KA or NMDA significantly...