Wan Q, Yang B S, Kato N
Department of Applied Biochemistry, Faculty of Applied Biological Science, Hiroshima University, Japan.
J Nutr Sci Vitaminol (Tokyo). 1996 Jun;42(3):185-93. doi: 10.3177/jnsv.42.185.
We have reported that excess cystine feeding exaggerates the defects of dietary copper deficiency in rats by a mechanism not involving oxidative stress and altered copper status. This study was conducted to examine whether this exacerbation is caused by a mechanism involving altered iron status and to compare the influences of cystine and cysteine feeding on the defects of copper deficiency. Male Wistar rats were fed copper-adequate or copper-deficient diet with supplementation of L-cystine or L-cysteine (2%) for 10 days or 21 days. Copper-deficient diet increased heart weight, caused anemia, reduced plasma iron and elevated liver iron. These defects were exacerbated by supplemental cystine. Cysteine feeding also exacerbated the defects of dietary copper deficiency including anemia, increased heart weight, and reduced plasma iron, although cysteine feeding had no influence on liver iron concentration. Supplemental cysteine reduced apparent absorption of iron, while supplemental cystine did not. These results suggest that cystine feeding enhances the defects of copper deficiency by a mechanism involving impaired mobilization of iron from liver into blood, and that cysteine feeding enhances the defects of copper deficiency by a mechanism involving reduced intestinal absorption of iron.
我们曾报道，过量饲喂胱氨酸会通过一种不涉及氧化应激和铜状态改变的机制，加剧大鼠饮食性铜缺乏的缺陷。本研究旨在检验这种加剧是否由一种涉及铁状态改变的机制引起，并比较饲喂胱氨酸和半胱氨酸对铜缺乏缺陷的影响。将雄性Wistar大鼠喂以含适量铜或铜缺乏的饲料，并补充L-胱氨酸或L-半胱氨酸（2%），持续10天或21天。铜缺乏饲料会增加心脏重量、导致贫血、降低血浆铁含量并升高肝脏铁含量。补充胱氨酸会加剧这些缺陷。饲喂半胱氨酸也会加剧饮食性铜缺乏的缺陷，包括贫血、心脏重量增加和血浆铁降低，尽管饲喂半胱氨酸对肝脏铁浓度没有影响。补充半胱氨酸会降低铁的表观吸收率，而补充胱氨酸则不会。这些结果表明，饲喂胱氨酸通过一种涉及肝脏中铁向血液中转运受损的机制增强铜缺乏的缺陷，而饲喂半胱氨酸通过一种涉及肠道铁吸收减少的机制增强铜缺乏的缺陷。
