儿童边缘性锌缺乏症综合判断的研究

对沈阳市某幼儿园９９例３～６岁锌缺乏儿童的营养调查和生物样品（血液、尿液和毛发）的分析发现：同对照组儿童相比，锌缺乏儿童除Ｆｅ、维生素Ａ外，其他主要营养素的摄入明显不足；缺锌儿童的发锌、ＲＢＣ锌水平、血清ＡＬＰ活性、尿锌／尿肌酐比值均明显低于对照组。经补锌治疗后血浆锌水平、血清ＡＬＰ活性、尿锌／尿肌酐比值显著升高。应用临床诊断实验的评价方法分析发现结合血浆锌水平，联合使用发锌，血清ＡＬＰ和尿锌／尿肌酐比值３项指标可以准确判断儿童边缘性锌缺乏，这时并联的灵敏度为９６．１８％，串联的特异度可高达到１００％（血清ＡＬＰ活性＜１０４ＩＵ／Ｌ，同时发锌含量＜１１０ｐｐｍ．尿锌／尿肌酐比值＜０．３μｇ／ｇ）。     

儿童锌缺乏敏感指标的评价

目的 为评价反映儿童锌缺乏的敏感指标。方法 我们对３００名３－６岁儿童进行膳食调查与体格检查，同时测定了锌缺乏组和对照儿童的尿肌酐比值。血清ＡＬＰ活性，血清胆固醇水平及锌缺乏儿童补锌治疗前后上述指标的变化。结果 锌缺乏组与姐尿锌与民酐幽会血清ＡＬＰ活性有显著性差异。锌缺乏组儿童血浆锌、尿锌与尿肌酐比值，血清ＡＬＰ活性，血清胆固醇水平在补锌治疗前后有显著性差异。结论 血浆锌和血清ＡＬＰ同时降低可以预     

儿童锌缺乏敏感指标的评价

为评价反映儿童锌缺乏的敏感指标.方法 我们对300名3～6岁儿童进行膳食调查与体格检查,同时测定了锌缺乏组和对照组儿童的尿锌与尿肌酐比值,血清ALP活性,血清胆固醇水平及锌缺乏儿童补锌治疗前后上述指标的变化.结果 锌缺乏组与对照组尿锌与尿肌酐比值,血清ALP活性有显著性差异.锌缺乏组儿童血浆锌,尿锌与尿肌酐比值,血清ALP活性,血清胆固醇水平在补锌治疗前后有显著性差异.结论 血浆锌和血清ALP同时降低可以预示儿童体内锌缺乏,需要补锌治疗;尿锌与尿肌酐比值能较敏感地反映儿童的锌营养状况;胆固醇与锌营养之间的关系值得进一步研究.     

接触二硫化碳工人血脂,血浆卵磷脂—胆固醇酰基转移酶活性…

本文对５７名接触二硫化碳工人和５５名非接触工人的血脂、血浆卵磷脂－胆固醇酰基转移酶活性及血清铜、锌值进行调查。结果表明；接触组工人血浆ＬＣＡＴ活性显著抑制（Ｐ＜０．０５），血清铜、锌值显著降低（Ｐ＜０．０５），血铜，锌比值增高（Ｐ＜０．０５）。血清铜、锌值与血脂及浆ＬＣＡＴ活性的线性相关分析无显著性。提示：ＣＳ２可通过抑制ＬＣＡＴ活性而引起脂质代谢障碍；ＣＳ２能干扰铜、锌代谢，导致机体铜、锌含量减     

儿童血清,头发,尿锌指标测定相关性分析

目的 为探讨儿童匀指标间的相关关系及补锌的有关问题。方法 对贵阳市６７名４－１２岁儿童同时测定血清、头发、尿锌浓度、口服０．２％硫酸锌３个月后复查。结果 ３种锌指标之间ｒ分别为０．０５００、０．３６９２、０．０４２０，Ｐ均〉０．０５，补锌后３项指标均明显升高，Ｐ〈０．０１，其中３７．５０％的学龄儿尿锌〉１５．３μｍｏｌ／Ｌ。结论 各锌指标之间无明显相关性，口服锌剂能有效改善儿童锌营养状况，但必须注     

二硫化碳作业工人血浆LCAT的测定

本文对血脂、肝功能均正常的８５名接触二硫化碳（ＣＳ＿２）工人和３６名不接触工人，均为男性，进行了血浆卵磷脂胆固醇酰基转移酶（ＬＣＡＴ）活力、血清铜、锌含量测定。结果表明：接触组工人ＬＣＡＴ活力、铜值、铜／锌比值显著低于对照组（Ｐ＜０．０５，Ｐ＜０．０５，Ｐ＜０．０１）；锌值未见统计学差异（Ｐ＞０．０５）。但ＬＣＡＴ活力与铜、锌、铜／锌比值线性相关分析未见明显相关。以上结果提示：长期接触高浓度ＣＳ＿２，在血脂未发生改变以前，可见ＬＣＡＴ活力、铜、铜／锌比值改变。以上指标作为ＣＳ＿２中毒诊断及健康监护有一定的应用价值。     

噪声对纺织女工血清铜,锌的影响

对１００例暴露于９６－１０２ｄＢ（Ａ）噪声环境的纺织女工和１００例对照组进行血清铜、锌含量测定，并计算铜／锌比值。结果显示：噪声组血清铜、锌含量均高于对照组（Ｐ＜０．０５）；而铜／锌比值则低于对照组（Ｐ＜０．０５），且铜、锌含量有随噪声暴露时间延长而增加的趋势。提示噪声这一有害物理因素可影响体内的微量元素水平，对进一步了解噪声的生物效应提供了依据。     

0～3岁儿童尿锌／尿肌酐比值与锌营养状况关系的临床研究

测定３２１名０～３岁儿童在不同性别、年龄、身高、体重条件下的尿锌／尿肌酐比值,以及５４名缺锌儿童补锌前后尿锌／尿肌酐比值的变化。结果：尿锌／尿肝比值男和女分别为１７８±０８６ｍｇ／ｇ、１７９±０９２ｍｇ／ｇ,１岁以下与１～３岁分别为１９０±１１２ｍｇ／ｇ,１７９±０８３ｍｇ／ｇ,均无显著性差异。高身高、高体重儿童测定值显著高于低身高、低体重儿童。补锌后尿锌／尿肌酐比值显著增高,但个体差异较大。可见尿锌／尿肌酐比值可作为评价机体锌营养状况的可靠指标。     

接触二硫化碳工人血脂、血浆卵磷脂─胆固醇酰基转移酶活性及血铜、锌值的调查

本文对５７名接触二硫化碳（ＣＳ＿２）工人和５５名非接触工人的血脂、血浆卵磷脂─胆固醇酰基转移酶（ＬＣＡＴ）活性及血清铜、锌值进行调查。结果表明：接触组工人血浆ＬＣＡＴ活性显著抑制（Ｐ＜０．０５），血清铜、锌值显著降低（Ｐ＜０．０５），血铜、锌比值增高（Ｐ＜０．０５）。血清铜、锌值与血脂及血浆ＬＣＡＴ活性的线性相关分析无显著性。揭示：ＣＳ＿２可通过抑制ＬＣＡＴ活性而引起脂质代谢障碍；ＣＳ＿２能干扰铜、锌代谢，导致机体铜、锌含量减少。但铜、锌含量减少与脂质代谢障碍的关系尚需进一步研究。     

氟致大鼠尿锌水平变化及对血浆SOD影响观察

用含１１０ｍｇ／Ｌ氟化钠的双蒸水饲养Ｗｉｓｔａｒｔ大鼠４周,检测大鼠尿锌、血浆锌和血浆ＳＯＤ水平。结果表明,实验组大鼠尿锌排泄量明显高于对照组（Ｐ＜０．０５）,血浆ＳＯＤ含量明显低于对照且（Ｐ＜０．０５）。     

Marginal zinc deficiency and changes in behavioral salt taste threshold and salt preference in mice

An animal model of marginal zinc deficiency was tested in mice, and salt taste threshold and salt preference were investigated in the state of marginal zinc deficiency. Two experiments were conducted. In Experiment 1, four-week-old male ICR mice were fed diets of three different levels of zinc content (3.17, 9.27, or 48.13 micrograms Zn/g) for 60 days. Food intake, growth, zinc levels in tissues, hepatic metallothionein (MT) content, and activities of selected enzymes (hepatic and RBC delta-amino-levulinic acid dehydratase (ALAD) and plasma alkaline phosphatase (ALP] did not differ among the groups throughout the experiment, and no overt signs of zinc deficiency were manifested in any group. In Experiment 2, four-week-old male ICR mice were fed a zinc-deficient diet (1.98 micrograms Zn/g) or a zinc-adequate diet (49.14 micrograms Zn/g) for 56 days. Food intake and growth did not differ between the two groups, and no overt signs of zinc deficiency were observed throughout the experiment. Zinc levels in the plasma and femur--but not those in the brain, kidneys, liver, and red blood cell (RBC)--and plasma ALP activities were significantly lower on Day 42 and Day 56 of the experiment in the mice fed the zinc-deficient diet (ZnD group) than in those fed the zinc-adequate diet (ZnA group). Hepatic MT contents were lower in the ZnD group than in the ZnA group on Day 56 only. Salt taste threshold was 0.05% in the ZnA group, while it was 0.1% in the ZnD group, between Day 30 and Day 38, and between Day 44 and Day 52 of the experiment. Preference for 0.9% NaCl solution was no different in the two groups when tested between Day 38 and Day 40 or between Day 52 and Day 54, but that for 1.6% NaCl solution was significantly higher in the ZnD group than in the ZnA group between Day 40 and Day 42, and between Day 54 and Day 56.     

Zinc Deficiency Blunts the Effectiveness of Antidepressants in the Olfactory Bulbectomy Model of Depression in Rats

Currently used antidepressants do not always provide the desired results, and many patients suffer from treatment-resistant depression. Clinical studies suggest that zinc deficiency (ZnD) may be an important risk factor for depression and might blunt the effect of antidepressants. This study aimed to examine whether ZnD might blunt the effectiveness of antidepressants in the olfactory bulbectomy model (OB) of depression in rats. For this purpose, rats were subjected to the OB model, fed a zinc-deficient diet (3 mg Zn/kg) for 3 weeks, and finally treated with escitalopram (Esc), venlafaxine (Ven) 10 mg/kg, i.p., or combined Esc/Ven (1 mg/kg, i.p.) with zinc (5 mg/kg) for another 3 weeks. Open field (OFT), forced swim (FST), and sucrose intake (SIT) tests were used to evaluate depressive-like behavioral changes. In addition, serum, intracellular, and synaptic Zn concentrations and the level of zinc transporter (ZnT) proteins were analyzed. The OB + ZnD model induced hyperactivity in rats in the OFT, increased immobility time in the FST, and anhedonia in the SIT. Chronic treatment with Esc reduced immobility time in the FST in the OB + ZnD model. Esc/Ven +Zn increased sucrose intake in rats from the OB + ZnD group. The OB + ZnD decreased serum zinc levels and intracellular and synaptic Zn concentration in the prefrontal cortex (PFC) and cerebellum. These changes were normalized by chronic administration of Esc/Ven +Zn. Moreover, OB + ZnD decreased levels of the ZnT1 protein in the PFC and Hp and ZnT3 in Hp. Chronic administration of antidepressants did not alter the levels of ZnT proteins. The OB + ZnD model induces more depressive-like effects than either model alone. Our results show that ZnD may induce drug resistance in rats. Normalizing serum or brain zinc concentration is insufficient to reverse behavioral abnormalities caused by the OB + ZnD model. However, zinc supplementation might improve the effectiveness of antidepressants in reversing particular depression symptoms.     

Prevalence of Zinc Deficiency in Healthy 1–3-Year-Old Children from Three Western European Countries

Zinc deficiency (ZnD) has adverse health consequences such as stunted growth. Since young children have an increased risk of developing ZnD, it is important to determine its prevalence and associated factors in this population. However, only a few studies have reported on ZnD prevalence in young children from Western high-income countries. This study evaluated ZnD prevalence and associated factors, including dietary Zn intake, in healthy 1–3-year-old children from Western European, high-income countries. ZnD was defined as serum Zn concentration <9.9 µmol/L. A total of 278 children were included with a median age of 1.7 years (Q1–Q3: 1.2–2.3). The median Zn concentration was 11.0 µmol/L (Q1–Q3: 9.0–12.2), and ZnD prevalence was 31.3%. No significant differences were observed in the socio-economic characteristics between children with and without ZnD. Dietary Zn intake was not associated with ZnD. ZnD is common in healthy 1–3-year-old children from Western European countries. However, the use of currently available cut-off values defining ZnD in young children has its limitations since these are largely based on reference values in older children. Moreover, these values were not evaluated in relation to health consequences, warranting further research.     

锌缺乏对大鼠骨骼肌α－肌动蛋白基因表达的影响

本文观察了缺锌对大鼠股四头肌深层肌总蛋白质、ＤＮＡ、总ＲＮＡ、肌动蛋白（ＤＮａｓｅⅠ抑制法）和α－肌动蛋白ｍＲＮＡ（地高辛标记探针，Ｎｏｒｔｈｅｒｎ杂交）含量的影响。结果显示：缺锌时肌肉中总蛋白质、ＤＮＡ和肌动蛋白的相对含量变化不明显，总ＲＮＡ和α－肌动蛋白ｍＲＮＡ的含量明显减少。这提示，锌缺乏导致α－肌动蛋白的基因表达下降，可能在转录和翻译过程中影响骨骼肌肌动蛋白的合成速率。     

Zn-depleted mice absorb more of an intragastric Zn solution by a metallothionein-enhanced process than do Zn-replete mice

The influence of metallothionein (MT)(2) on Zn absorption was investigated in MT-null (MT-/-) and normal (MT+/+) mice fed Zn-depleted (ZnD) diets for 7 d and compared with those fed Zn-replete (ZnR) diets in a previous study. Mice were starved for 20 h, then administered an oral gavage of aqueous (65)ZnSO(4) solution at doses of 154, 770 or 1540 nmol of Zn, and the amount transferred into nongut tissues was determined 4 h later. (65)Zn transfer did not differ between genotypes in ZnR mice. However ZnD MT+/+ mice had a 30-40% greater transfer from the 154 and 770 Zn doses compared to ZnR MT+/+ mice. This was not observed in MT-/- mice. In MT+/+ mice, Zn depletion enhanced the induction of MT by Zn in the intestine and pancreas. (65)Zn uptakes in the liver and pancreas were greater in MT+/+ than MT-/- mice, and this was greater (50%) at the 154 and 770 doses in mice fed ZnD diets. Plasma Zn concentrations were raised to a similar extent in ZnR and ZnD MT-/- mice. ZnR MT+/+ mice had significantly lower plasma Zn levels than MT-/-mice; this difference was less marked in the ZnD mice. We conclude that a MT-facilitated enhancement in Zn absorption occurs in response to dietary Zn deficiency.     

儿童骨密度与血清硒、锌、钙、铅及碱性磷酸酶水平的关系:附95例报告

目的探讨儿童骨密度(BMD)降低与血清硒(Se)、锌(Zn)、铁(Fe)、钙(Ca)、铅(Pb)及碱性磷酸酶(ALP)水平的关系。方法采用双能X线骨密度仪检测BMD,石墨炉原子吸收法检测血铅,荧光分光光度法检测血硒,等离子体火焰光谱法(ICP)检测血锌,亚铁嗪比色法检测血清铁,偶氮砷Ⅲ染色法检测血钙,速率法测ALP。结果低BMD组血铅水平明显高于对照组(P<0.01),且达轻度铅中毒水平;而血清硒、铁则明显低于对照组(P<0.05);血锌水平两组间差异无显著性(P>0.05)。低BMD组中血钙及ALP同时增高者占73%,显著高于对照组的11.1%。结论儿童低BMD与高血铅、低血硒、低血清铁有一定关联;而血钙与血ALP同时增高可为早期发现低BMD提供有利诊察线索。     

锌,硒单独与联合作用对镉毒性拮抗作用的研究

本研究对镉，锌，硒单独或同时给与时相互之间的作用及影响进行了测定，以观察锌，硒对镉毒性的拮抗，实验中把４０只Ｗｉｓｔａｒ大鼠分为镉，镉锌，镉硒，镉锌硒及对照共五组，观察指标为大鼠体重变化；血清，镉，硒，锌；尿：镉，硒，锌；尿蛋白及血清碱性磷酸酶（ＡＫＰ），结果进行统计学处理后表明：加入锌，硒后，镉中毒的大鼠体重回升，血镉下降，尿蛋白下降，血清ＡＫＰ回升，尿镉排出增加，提示锌，硒对镉中毒表现有拮抗作     

The analysis of stable isotopes in urine to determine the fractional absorption of zinc.

We measured isotopic enrichment in urine after oral and intravenous administration of stable isotopes of zinc to determine fractional absorption (FA). 68Zn and 70Zn were administered orally and intravenously to four normal adults. Subsequently, urine and fecal samples were collected for 7 and 14 d, respectively, ashed, and passed through ion-exchange columns to separate zinc from other elements. Samples were analyzed by fast-atom-bombardment mass spectrometry. From 32 h onwards the enrichment of 68Zn and 70Zn in urine declined proportionately so that FA could be determined as follows: FA = enrichment (oral/iv) x dose (iv/oral). FA determinations from urine and feces (cumulative excretion) were, respectively, for subject ZK1, urine 0.79 +/- 0.03 and feces 0.70 +/- 0.01; ZK2, 0.79 +/- 0.05 and 0.69 +/- 0.02; ZK3, 0.26 +/- 0.01 and 0.25 +/- 0.01; and ZK4, 0.41 +/- 0.02 and 0.37 +/- 0.02. ZK1 and ZK2 received the oral isotope while fasting whereas ZK3 and ZK4 received the oral isotope with meals. FA of zinc can be determined by measurement of isotope enrichment in urine.     

Effect of experimental zinc deficiency and repletion on sodium, potassium, copper and iron concentrations in guinea-pigs

Zinc, sodium, potassium, copper and iron concentrations were analysed in serum and tissues of guinea-pigs fed on a diet containing 1.25 mg Zn/kg diet over a period of 60 d. The response of the Zn-deficient (ZnD) animals to Zn supplementation (100 mg Zn/kg diet) was also studied for 15 d. Serum studies in the ZnD group revealed significant decreases in the concentrations of Zn and Na from 24 d, and increases in the concentrations of Fe and K from 36 and 48 d onwards respectively; an increase in Cu was seen on day 60 only. Zn deficiency caused significant reductions in Na, K and Zn and increases in Cu and Fe contents of liver and kidney. In testis, significant decreases were noted only in Zn, K and Fe contents. Zn supplementation of the previously ZnD group resulted in marked improvements in serum and tissue mineral levels. However, hepatic Cu and Fe and renal K did not appear to respond appreciably.