Cardoso Henriqueta D, Passos Priscila P, Lagranha Claudia J, Ferraz Anete C, Santos Júnior Eraldo F, Oliveira Rafael S, Oliveira Pablo E L, Santos Rita de C F, Santana David F, Borba Juliana M C, Rocha-de-Melo Ana P, Guedes Rubem C A, Navarro Daniela M A F, Santos Geanne K N, Borner Roseane, Picanço-Diniz Cristovam W, Beltrão Eduardo I, Silva Janilson F, Rodrigues Marcelo C A, Andrade da Costa Belmira L S
Laboratório de Neurofisiologia, Departamento de Fisiologia e Farmacologia, Centro de Ciências Biológicas, Universidade Federal de Pernambuco Recife, Brazil.
Front Hum Neurosci. 2012 Aug 30;6:249. doi: 10.3389/fnhum.2012.00249. eCollection 2012.
Oxidative stress (OS) has been implicated in the etiology of certain neurodegenerative disorders. Some of these disorders have been associated with unbalanced levels of essential fatty acids (EFA). The response of certain brain regions to OS, however, is not uniform and a selective vulnerability or resilience can occur. In our previous study on rat brains, we observed that a two-generation EFA dietary restriction reduced the number and size of dopaminergic neurons in the substantia nigra (SN) rostro-dorso-medial. To understand whether OS contributes to this effect, we assessed the status of lipid peroxidation (LP) and anti-oxidant markers in both SN and corpus striatum (CS) of rats submitted to this dietary treatment for one (F1) or two (F2) generations. Wistar rats were raised from conception on control or experimental diets containing adequate or reduced levels of linoleic and α-linolenic fatty acids, respectively. LP was measured using the thiobarbituric acid reaction method (TBARS) and the total superoxide dismutase (t-SOD) and catalase (CAT) enzymatic activities were assessed. The experimental diet significantly reduced the docosahexaenoic acid (DHA) levels of SN phospholipids in the F1 (28%) and F2 (50%) groups. In F1 adult animals of the experimental group there was no LP in both SN and CS. Consistently, there was a significant increase in the t-SOD activity (p < 0.01) in both regions. In EF2 young animals, degeneration in dopaminergic and non-dopaminergic neurons and a significant increase in LP (p < 0.01) and decrease in the CAT activity (p < 0.001) were detected in the SN, while no inter-group difference was found for these parameters in the CS. Conversely, a significant increase in t-SOD activity (p < 0.05) was detected in the CS of the experimental group compared to the control. The results show that unbalanced EFA dietary levels reduce the redox balance in the SN and reveal mechanisms of resilience in the CS under this stressful condition.
氧化应激（OS）与某些神经退行性疾病的病因有关。其中一些疾病与必需脂肪酸（EFA）水平失衡有关。然而，某些脑区对OS的反应并不一致，可能会出现选择性易损性或恢复力。在我们之前对大鼠大脑的研究中，我们观察到两代EFA饮食限制减少了黑质（SN） rostro-dorso-medial中多巴胺能神经元的数量和大小。为了了解OS是否导致了这种效应，我们评估了接受一代（F1）或两代（F2）这种饮食处理的大鼠SN和纹状体（CS）中脂质过氧化（LP）和抗氧化标志物的状态。Wistar大鼠从受孕开始就分别饲养在含有充足或降低水平的亚油酸和α-亚麻酸的对照或实验饮食中。使用硫代巴比妥酸反应法（TBARS）测量LP，并评估总超氧化物歧化酶（t-SOD）和过氧化氢酶（CAT）的酶活性。实验饮食显著降低了F1（约28%）和F2（约50%）组中SN磷脂的二十二碳六烯酸（DHA）水平。在实验组的F1成年动物中，SN和CS中均未检测到LP。一致地，两个区域的t-SOD活性均显著增加（p < 0.01）。在EF2幼龄动物中，SN中检测到多巴胺能和非多巴胺能神经元的退化以及LP显著增加（p < 0.01）和CAT活性降低（p < 0.001），而CS中这些参数在组间未发现差异。相反，与对照组相比，实验组CS中的t-SOD活性显著增加（p < 0.05）。结果表明，EFA饮食水平失衡会降低SN中的氧化还原平衡，并揭示了在这种应激条件下CS中的恢复机制。
