White C L
Institute for Nutritional Physiology, Technical University of Munich, Freising-Weihenstephan, F.R.G.
Aust J Biol Sci. 1988;41(3):343-56. doi: 10.1071/bi9880343.
Recent evidence suggests that changes in plasma zinc concentration may play a central role in the development of early lesions of zinc deficiency. The aim of the following work was to better understand events occurring in plasma during the onset of zinc deficiency, and to investigate biochemical mechanisms by which plasma zinc may exert its effects. Fifty male weanling rats of 90 g weight were allocated to five treatment groups of ten rats each. Treatments were: 1, zinc deficient, mixed diet (1-2 mg Zn per kg): 2, zinc deficient, self-select diet; 3, zinc repleted; 4, control, pair fed; 5, control, ad libitum fed. With the exception of treatment 1, which consisted of a 25% casein diet, all rats were offered protein as a separate component of the diet. Control rats received zinc in the drinking water (100 mg l-1). The sequence of events following initiation of zinc deficiency were: reduced plasma zinc concentration (2 days), reduced plasma angiotensin-converting enzyme and alkaline phosphatase activities (3-4 days), reduced feed intake and growth (5-6 days) and reduced percentage protein intake (12 days). Plasma zinc concentration in the deficient rats was inversely correlated with the growth rate of the rat over the previous 24 h. Zinc repletion resulted in marked overshoot in plasma zinc concentration (300%) and converting-enzyme activity (150%) within 24 h, but a return to normal within 72 h. Alkaline phosphatase activity responded likewise, albeit more slowly. Protein self selection had no effect on the manifestations of zinc deficiency, although reduced protein intake was associated with lower plasma zinc concentration. The results provide evidence of a role for plasma zinc in the development of early clinical signs of zinc deficiency, possibly acting biochemically through reduced activity of zinc-dependent peptidases such as angiotensin-converting enzyme.
近期证据表明，血浆锌浓度的变化可能在锌缺乏早期病变的发展中起核心作用。以下工作的目的是更好地了解锌缺乏开始时血浆中发生的事件，并研究血浆锌发挥其作用的生化机制。将50只体重90克的雄性断奶大鼠分为五个治疗组，每组10只。治疗方法如下：1. 锌缺乏，混合饮食（每千克含1 - 2毫克锌）；2. 锌缺乏，自选饮食；3. 锌补充；4. 对照，配对喂养；5. 对照，自由采食。除了由25%酪蛋白饮食组成的治疗组1外，所有大鼠的蛋白质均作为饮食的单独成分提供。对照大鼠在饮用水中摄入锌（100毫克/升）。锌缺乏开始后的事件顺序为：血浆锌浓度降低（2天）、血浆血管紧张素转换酶和碱性磷酸酶活性降低（3 - 4天）、采食量和生长量降低（5 - 6天）以及蛋白质摄入量百分比降低（12天）。缺锌大鼠的血浆锌浓度与大鼠前24小时的生长速率呈负相关。补锌后，血浆锌浓度（300%）和转换酶活性（150%）在24小时内显著超调，但在72小时内恢复正常。碱性磷酸酶活性的反应类似，尽管较慢。蛋白质自选对锌缺乏的表现没有影响，尽管蛋白质摄入量降低与较低的血浆锌浓度有关。结果提供了证据，表明血浆锌在锌缺乏早期临床症状的发展中起作用，可能通过降低锌依赖性肽酶（如血管紧张素转换酶）的活性发挥生化作用。
