Santos R X, Cardoso S, Silva S, Correia S, Carvalho C, Crisóstomo J, Rodrigues L, Amaral C, Louro T, Matafome P, Santos M S, Proença T, Duarte A I, Seiça R, Moreira P I
Dept. of Zoology, Coimbra Univ. Hospital, Univ. of Coimbra, Portugal.
J Food Sci. 2009 Jan-Feb;74(1):H8-H14. doi: 10.1111/j.1750-3841.2008.00982.x.
The present study was aimed to evaluate the effect of food deprivation in brain oxidative status of Wistar and Goto-Kakizaki (GK) rats. For this purpose, we evaluated several oxidative stress parameters: lipid peroxidation (thiobarbituric acid reactive substances [TBARS]) and protein oxidation markers, hydrogen peroxide (H(2)O(2)) levels, nonenzymatic (reduced [GSH] and oxidized glutathione [GSSG] and vitamin E) and enzymatic (glutathione peroxidase [GPx], glutathione reductase [GRed], and manganese superoxide dismutase [MnSOD]) antioxidant defenses. Four-mo-old Wistar and GK rats were divided into 2 groups. One group of each rat strain was maintained under normal diet and the other groups were maintained under 50% food deprivation during 2 mo. GK rats under normal diet presented lower levels of vitamin E and higher GRed activity and GSH/GSSG ratio when compared with Wistar control rats. In Wistar rats, food deprivation induced a significant decrease in vitamin E levels and a significant increase in GPx activity, H(2)O(2) production, and TBARS formation in the presence of the prooxidant pair ADP/Fe(2+). However, GK rats under food deprivation presented a significant decrease in vitamin E levels and GRed activity and a significant increase in H(2)O(2) production when compared with GK under normal diet. In summary, our results indicate that food deprivation affects brain oxidative status, which could predispose brain cells to degeneration and death.
本研究旨在评估食物剥夺对Wistar大鼠和Goto-Kakizaki(GK)大鼠脑氧化状态的影响。为此,我们评估了几个氧化应激参数:脂质过氧化(硫代巴比妥酸反应性物质[TBARS])和蛋白质氧化标志物、过氧化氢(H₂O₂)水平、非酶抗氧化剂(还原型谷胱甘肽[GSH]、氧化型谷胱甘肽[GSSG]和维生素E)以及酶抗氧化剂(谷胱甘肽过氧化物酶[GPx]、谷胱甘肽还原酶[GRed]和锰超氧化物歧化酶[MnSOD])防御能力。4月龄的Wistar大鼠和GK大鼠被分为两组。每种大鼠品系的一组维持正常饮食,另一组在2个月内维持50%食物剥夺状态。与Wistar对照大鼠相比,正常饮食的GK大鼠维生素E水平较低,GRed活性较高,GSH/GSSG比值较高。在Wistar大鼠中,食物剥夺导致维生素E水平显著降低,在存在促氧化剂对ADP/Fe²⁺的情况下,GPx活性、H₂O₂产生和TBARS形成显著增加。然而,与正常饮食的GK大鼠相比,食物剥夺的GK大鼠维生素E水平和GRed活性显著降低,H₂O₂产生显著增加。总之,我们的结果表明食物剥夺会影响脑氧化状态,这可能使脑细胞易发生变性和死亡。