Ziegler Denize R, Ribeiro Leticia C, Hagenn Martine, Siqueira Ionara R, Araújo Emeli, Torres Iracy L S, Gottfried Carmem, Netto Carlos Alexandre, Gonçalves Carlos-Alberto
Centro de Ciências da Saúde, Universidade do Vale do Rio dos Sinos, São Leopoldo, RS, Brazil.
Neurochem Res. 2003 Dec;28(12):1793-7. doi: 10.1023/a:1026107405399.
Ketogenic diets have been used in the treatment of refractory childhood epilepsy for almost 80 years; however, we know little about the underlying biochemical basis of their action. In this study, we evaluate oxidative stress in different brain regions from Wistar rats fed a ketogenic diet. Cerebral cortex appears to have not been affected by this diet, and cerebellum presented a decrease in antioxidant capacity measured by a luminol oxidation assay without changes in antioxidant enzyme activities--glutathione peroxidase, catalase, and superoxide dismutase. In the hippocampus, however, we observed an increase in antioxidant activity accompanied by an increase of glutathione peroxidase (about 4 times) and no changes in lipoperoxidation levels. We suggest that the higher activity of this enzyme induced by ketogenic diet in hippocampus might contribute to protect this structure from neurodegenerative sequelae of convulsive disorders.
生酮饮食已用于治疗难治性儿童癫痫近80年；然而，我们对其作用的潜在生化基础知之甚少。在本研究中，我们评估了喂食生酮饮食的Wistar大鼠不同脑区的氧化应激。大脑皮层似乎未受这种饮食影响，而小脑通过鲁米诺氧化测定法测得的抗氧化能力下降，抗氧化酶活性（谷胱甘肽过氧化物酶、过氧化氢酶和超氧化物歧化酶）未发生变化。然而，在海马体中，我们观察到抗氧化活性增加，同时谷胱甘肽过氧化物酶增加（约4倍），脂质过氧化水平无变化。我们认为，生酮饮食在海马体中诱导的该酶较高活性可能有助于保护该结构免受惊厥性疾病的神经退行性后遗症影响。
