Nkabyo Yvonne S, Gu Li H, Jones Dean P, Ziegler Thomas R
Department of Medicine, Emory University, Atlanta, GA 30322, USA.
J Nutr. 2006 May;136(5):1242-8. doi: 10.1093/jn/136.5.1242.
Low molecular weight thiol/disulfide redox pools are dependent upon extracellular cysteine (Cys) availability. We determined whether dietary sulfur amino acid (SAA) deficiency induces oxidative stress in vivo, as determined by redox state of major thiol/disulfide couples in plasma [Cys/cystine (CySS)] and intestinal mucosa [glutathione (GSH)/glutathione disulfide (GSSG)]. Rats were fed isocaloric, isonitrogenous semipurified diets: either SAA-adequate (control), SAA-deficient, or SAA-supplemented, pair-fed to intake of the SAA-deficient group. Reference rats consumed standard rat food ad libitum. After 7 d, plasma and gut mucosal samples were analyzed for Cys, CySS, GSH and GSSG, and the redox potentials of Cys/CySS and GSH/GSSG were determined. Mean daily food intake in the pair-fed rats was similar (approximately one-half of reference-rat intake). Body weight decreased in all pair-fed groups, but rats fed the SAA-deficient diet lost significantly more body weight. Dietary SAA deficiency decreased GSH concentrations in both plasma and gut mucosa, increased plasma GSSG, and oxidized plasma and gut mucosal GSH/GSSG redox and plasma Cys/CySS redox. SAA supplementation resulted in a more reducing plasma Cys/CySS redox potential. Reference rats exhibited similar tissue and plasma GSH/GSSG redox as rats that ate semipurified SAA-adequate rat food, which provided similar net SAA intake. Our in vivo data show that inadequate dietary SAA intake oxidizes the thiol/disulfide redox status in rat-gut mucosa and plasma. Such oxidation of redox pools is associated with oxidative stress and the onset or progression of several pathological conditions. Thus, dietary SAA deficiency could contribute to the progression of disease by causing an oxidation of these components.
低分子量硫醇/二硫化物氧化还原池取决于细胞外半胱氨酸（Cys）的可用性。我们通过血浆中主要硫醇/二硫化物对[Cys/胱氨酸（CySS）]和肠黏膜中[谷胱甘肽（GSH）/谷胱甘肽二硫化物（GSSG）]的氧化还原状态，来确定饮食中硫氨基酸（SAA）缺乏是否会在体内诱导氧化应激。给大鼠喂食等热量、等氮的半纯化日粮：要么是SAA充足（对照）、SAA缺乏，要么是补充SAA，并按SAA缺乏组的摄入量进行配对喂养。对照大鼠随意食用标准大鼠食物。7天后，分析血浆和肠道黏膜样本中的Cys、CySS、GSH和GSSG，并测定Cys/CySS和GSH/GSSG的氧化还原电位。配对喂养大鼠的平均每日食物摄入量相似（约为对照大鼠摄入量的一半）。所有配对喂养组的体重均下降，但喂食SAA缺乏日粮的大鼠体重下降明显更多。饮食中SAA缺乏会降低血浆和肠道黏膜中的GSH浓度，增加血浆GSSG，并使血浆和肠道黏膜中的GSH/GSSG氧化还原以及血浆Cys/CySS氧化还原发生改变。补充SAA会使血浆Cys/CySS氧化还原电位更趋于还原状态。对照大鼠的组织和血浆GSH/GSSG氧化还原状态与食用半纯化SAA充足大鼠食物的大鼠相似，后者提供了相似的净SAA摄入量。我们的体内数据表明，饮食中SAA摄入不足会使大鼠肠道黏膜和血浆中的硫醇/二硫化物氧化还原状态发生改变。这种氧化还原池的氧化与氧化应激以及几种病理状况的发生或进展有关。因此，饮食中SAA缺乏可能会通过导致这些成分的氧化而促进疾病的进展。
