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丘脑超氧化物和过氧化物处理能力(SPHC):铝、乙醇和生育酚对大鼠影响的实验研究

Thalamic superoxide and peroxide handling capacity (SPHC): An experimental study with aluminum, ethanol and tocopherol in rats.

作者信息

Nayak Prasunpriya, Sharma S B, Chowdary N V S

出版信息

Indian J Exp Biol. 2015 Sep;53(9):568-73.

PMID:26548076
Abstract

Superoxide and peroxide handling capacity (SPHC) is an important determinant of oxidative stress. Neurotoxic impacts of aluminum are associated with oxidant imbalance. Here, we studied the influence of aluminum on oxidative stress parameters, antioxidative enzymes and SPHC of thalamic area on pro-oxidant (ethanol) and antioxidant (α-tocopherol) exposure. Two sets of male Wistar rats were divided into 8 groups (6 each) and exposed to aluminum (10 mg/Kg body wt.), ethanol (0.6 g/Kg body wt.) and α-tocopherol (5 IU/day) for 4 wk, each having respective control group. Levels of reduced glutathione (GSH), lipid peroxidation (TBARS) along with activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione reductase (GR) of thalamic area were estimated for each group. Glutathione-independent superoxide peroxide handling capacity (GI-SPHC) and glutathione-dependent superoxide peroxide handling capacity (GD-SPHC) were calculated from the GPx, CAT and SOD values. Concomitant exposure to aluminum and ethanol demonstrated significant increase in SOD activity and significant decrease in GPx activity compared to the control group, while lone aluminum-exposed rats showed raised GR activity, without alterations in GPx and SOD activities. However, significant reduction of both GI- and GD- SPHC were found in ethanol-exposed groups. α-Tocopherol supplementation could resist most of the alterations. In addition, current antioxidant exposure reduced the inherent GD-SPHC, and thus, made thalamic area more vulnerable to oxidant threat. The present study corroborates the thalamic susceptibility to aluminum-augmented oxidant imbalance and suggests cautious use of antioxidant supplementation against neurodegenerative disorders.

摘要

超氧化物和过氧化物处理能力(SPHC)是氧化应激的一个重要决定因素。铝的神经毒性影响与氧化剂失衡有关。在此,我们研究了铝对丘脑区域氧化应激参数、抗氧化酶和SPHC在暴露于促氧化剂(乙醇)和抗氧化剂(α-生育酚)时的影响。将两组雄性Wistar大鼠分为8组(每组6只),并暴露于铝(10毫克/千克体重)、乙醇(0.6克/千克体重)和α-生育酚(5国际单位/天)4周,每组均有各自的对照组。对每组丘脑区域的还原型谷胱甘肽(GSH)水平、脂质过氧化(TBARS)以及超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GPx)和谷胱甘肽还原酶(GR)的活性进行了评估。根据GPx、CAT和SOD的值计算了非谷胱甘肽依赖性超氧化物过氧化物处理能力(GI-SPHC)和谷胱甘肽依赖性超氧化物过氧化物处理能力(GD-SPHC)。与对照组相比,铝和乙醇同时暴露组的SOD活性显著增加,GPx活性显著降低,而单独暴露于铝的大鼠GR活性升高,GPx和SOD活性无变化。然而,在乙醇暴露组中发现GI-SPHC和GD-SPHC均显著降低。补充α-生育酚可以抵抗大多数变化。此外,当前的抗氧化剂暴露降低了固有的GD-SPHC,因此,使丘脑区域更容易受到氧化剂威胁。本研究证实了丘脑对铝增强的氧化剂失衡的易感性,并建议谨慎使用抗氧化剂补充剂来对抗神经退行性疾病。

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