Oxidative stress and antioxidant defenses after prolonged starvation in Dentex dentex liver
Oxidative stress and antioxidant defenses after prolonged starvation in Dentex dentex liver
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DOI：
10.1016/j.cca.2004.10.008
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发表时间：
2004-10-01
影响因子：
3.9
通讯作者：
Cardenete, G
中科院分区：
文献类型：
--
作者：
Morales, AE;Pérez-Jiménez, A;Cardenete, G
本研究旨在探讨长时间饥饿和再摄食对普通牙体抗氧化状态和一些代谢相关参数的影响。（牙齿）肝脏。被剥夺食物5周的鱼显示出脂质过氧化的显著增加，测量为丙二醛（MDA）水平。与对照组相比，饥饿鱼体内抗氧化酶超氧化物歧化酶（SOD）、过氧化氢酶（过氧化氢酶）和谷胱甘肽过氧化物酶（GPX）活性显著升高（分别提高42%、22%和52%），而谷胱甘肽还原酶（GR）活性显著降低53%。非变性PAGE分析未发现SOD同工酶模式发生质的变化，但CuZn-SOD I和II对应的同工酶在饥饿鱼中增强。氧化代谢酶对羟基辅酶a脱氢酶（HOAD）和柠檬酸合成酶（CS）活性显著提高（分别提高123%和28%），葡萄糖-6-磷酸脱氢酶（G6PDH）活性降低56%。在这种情况下，氧化损伤是可逆的，因为所有生物标志物在重新喂食后恢复到控制值。我们的研究结果表明，尽管激活了抗氧化防御机制，但长期饥饿会导致促氧化情况和氧化应激，并且抑制G6PDH活性可能是细胞抗氧化防御失败的原因。(C) 2004爱思唯尔公司版权所有。
The aim of this work was to evaluate the effects of prolonged starvation and refeeding on antioxidant status and some metabolic-related parameters in common dentex. (Dentex dentex) liver. Fish deprived of food for 5 weeks showed a significant increase in lipid peroxidation, measured as malondialdehyde (MDA) levels. The activity of the antioxidative enzymes superoxide dismutase (SOD), catalase, and glutathione peroxidase (GPX) in starved fish significantly increased (by 42%, 22%, and 52%, respectively), whereas glutathione reductase (GR) activity was significantly depressed by 53% compared to controls. No qualitative changes in the SOD isoenzymatic pattern were detected by nondenaturing PAGE analysis, but the isoforms corresponding to CuZn-SOD I and II were enhanced in starved fish. The activity of the enzymes indicative of oxidative metabolism, p-hydroxyacyl CoA dehydrogenase (HOAD) and citrate synthase (CS), significantly increased (by 123% and 28%, respectively), and that of glucose-6-phosphate dehydrogenase (G6PDH) was inhibited by 56%. Oxidative damage under these circumstances is reversible since all biomarkers assayed returned to control values after refeeding. Our results show that prolonged starvation leads to a pro-oxidant situation and oxidative stress despite activation of antioxidant defense mechanisms, and that inhibition of G6PDH activity might be responsible for this failure in cellular antioxidant defenses. (C) 2004 Elsevier Inc. All rights reserved.