Gottschall-Pass K T, Grahn B H, Gorecki D K, Paterson P G
College of Pharmacy and Nutrition, University of Saskatchewan, Saskatoon, Canada.
J Nutr. 1997 Jun;127(6):1206-13. doi: 10.1093/jn/127.6.1206.
Our objective was to investigate whether zinc interacts with taurine to influence the development of retinal structure and function. Virgin female Sprague-Dawley rats were bred overnight and assigned to one of four treatments in a 2 x 2 factorial design with two levels of zinc (50 micrograms/g through gestation and 50 micrograms/g after parturition; 15 micrograms/g through gestation and 7.5 micrograms/g after parturition) and two levels of taurine (2 or 0 mumol/g). The control diet contained 50 micrograms/g zinc and 2 mumol/g taurine. Guanidinoethyl sulfonate (10 g/L), a taurine transport inhibitor, was added to the drinking water of the rats receiving 0 mumol/g taurine. At postnatal d 23, male pups (n = 10) were weaned onto their respective diets. Pup eyes were examined by biomicroscope and indirect ophthalmoscope at 4 and 7 wk; retinal folds and choroidal atrophy were detected in the pups deficient in zinc and taurine. Analysis of plasma zinc and tibial zinc concentrations revealed a significant interaction in these tissues (P < 0.05). Dark-adapted oscillatory potentials (OP) were recorded at 7.5-8.5 wk. Two-way ANOVA showed a significant interaction between zinc and taurine for OP2 and OP3 amplitudes; marginal zinc deficiency decreased the amplitude of the OP only when rats were also deficient in taurine. A significant depressing effect of marginal zinc deficiency was noted for OP1 amplitude. Taurine deficiency significantly depressed the amplitude of OP1 and OP4. Histological examination of the retinas from rats deficient in both zinc and taurine revealed photoreceptor degeneration and confirmed retinal dysplasia. These data provide evidence for an interaction between zinc and taurine in retinal morphology and function.
我们的目的是研究锌是否与牛磺酸相互作用,以影响视网膜结构和功能的发育。将未交配的雌性斯普拉格-道利大鼠饲养过夜,并按照2×2析因设计分为四种处理组之一,该设计有两个锌水平(妊娠期50微克/克,产后50微克/克;妊娠期15微克/克,产后7.5微克/克)和两个牛磺酸水平(2或0微摩尔/克)。对照饮食含有50微克/克锌和2微摩尔/克牛磺酸。将牛磺酸转运抑制剂胍基乙磺酸盐(10克/升)添加到接受0微摩尔/克牛磺酸的大鼠饮用水中。在出生后第23天,雄性幼崽(n = 10)断奶并喂食各自的饮食。在4周和7周时,用生物显微镜和间接检眼镜检查幼崽的眼睛;在锌和牛磺酸缺乏的幼崽中检测到视网膜褶皱和脉络膜萎缩。血浆锌和胫骨锌浓度分析显示这些组织中存在显著的相互作用(P < 0.05)。在7.5 - 8.5周时记录暗适应振荡电位(OP)。双向方差分析显示锌和牛磺酸对OP2和OP3振幅有显著的相互作用;仅当大鼠也缺乏牛磺酸时,边缘性锌缺乏才会降低OP的振幅。边缘性锌缺乏对OP1振幅有显著的抑制作用。牛磺酸缺乏显著降低了OP1和OP4的振幅。对锌和牛磺酸均缺乏的大鼠视网膜进行组织学检查,发现光感受器退化并证实存在视网膜发育异常。这些数据为锌和牛磺酸在视网膜形态和功能方面的相互作用提供了证据。