丙二醛
抗坏血酸
脂质过氧化
抗氧化剂
生理盐水
化学
内分泌学
内科学
药理学
麻醉
医学
生物化学
食品科学
作者
Rosângela Figueiredo Mendes-da-Silva,Andreia Morais,Maria Eduarda Bandim-da-Silva,Gabriela de Araujo Cavalcanti,Ana Rafaela Oliveira Rodrigues,Belmira Lara da Silveira Andrade‐da‐Costa,Rubem Carlos Araújo Guedes
标识
DOI:10.1016/j.neuropharm.2014.06.027
摘要
Although ascorbic acid (AA) is an antioxidant, under certain conditions it can facilitate oxidation, which may underlie the opposite actions of AA on brain excitability in distinct seizure models. Here, we investigated whether chronic AA administration during brain development alters cortical excitability as a function of AA dose, as indexed by cortical spreading depression (CSD) and by the levels of lipid peroxidation-induced malondialdehyde. Well-nourished and early-malnourished rats received per gavage 30, 60, or 120 mg/kg/d of AA, saline, or no gavage treatment (naïve group) at postnatal days 7–28. CSD propagation and malondialdehyde levels were analyzed at 30–40 days. Confirming previous observations, CSD velocities were significantly higher in the early-malnourished groups than in the well-nourished groups. AA dose was important: 30 mg/kg/d AA decelerated CSD and reduced malondialdehyde levels, whereas 60 mg/kg/d and 120 mg/kg/d accelerated CSD and augmented malondialdehyde levels compared with the corresponding saline and naïve groups. Our findings reinforce previous suggestion that AA acts as an antioxidant in the brain when administered at low doses, but as a prooxidant at high doses, as indicated by CSD propagation and malondialdehyde levels.
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