锌缺乏对儿童智力发育的影响

目的研究儿童锌缺乏与智力发育的关系.方法根据儿童的临床表现将其分为正常对照组、无症状缺锌组、有症状缺锌组;治疗前后利用原子吸收法分别测定各组血清锌含量并测其智商水平;将血清锌与智商水平进行相关分析;比较补锌治疗前后智商的变化.结果两缺锌组儿童补锌前平均血锌水平较对照组血锌含量低(P＜0.01);无症状缺锌组血锌水平稍高于有症状缺锌组(P＜0.01);血锌值与智商呈正相关关系(r=0.325,P＜0.01),n=100);两缺锌组儿童智商水平较正常儿童组低(P＜0.01);无症状缺锌组儿童智商值较有症状缺锌组儿童稍高,但无统计学意义(P＞0.05);正常对照组儿童的智商值明显高于缺锌组儿童(P＜0.01).补锌治疗后,两缺锌组儿童血锌水平较以前明显提高(P＜0.01),与正常对照组之间无统计学差异(P＞0.05);两缺锌组儿童智商水平都有明显的提高(P＜0.01).结论锌是影响儿童智力发育的一个比较重要影响因素,缺锌可影响智力发育;在一定范围内,这种影响是可逆的,经补锌后可以逆转.加强缺锌的预防,对缺锌的儿童及时进行补锌治疗,可改善儿童智力发育.     

锌缺乏与过量对体外培养的小鼠胚胎肢芽发育的影响

目的:观察锌缺乏与过量对体外培养的小鼠胚胎肢芽发育的影响,为锌的合理营养提供实验依据。方法:应用恒温旋转胚胎培养箱对12 d孕龄小鼠胚胎前肢芽进行培养,观察锌缺乏与过量对胚胎肢芽发育的影响,并进行Neubert评分。结果:锌浓度为43.0~86.0μmol/L时,对胚胎肢芽发育具有明显的促进作用;锌缺乏(0.0μmol/L)能导致胚胎肢芽发育评分下降,肢芽细胞分化,组织器官形态分化均受到不同程度抑制;锌过量(172.0~215μmol/L以上)时,能使VYS血管形成及神经系统、心脏、肢芽的器官形态分化受抑,所有生长发育和组织器官形态分化指标值均明显低于对照组(P<0.05);肢芽各软骨的发育分化差,Neubert评分少。结论:锌缺乏和锌过量均可影响小鼠胚胎肢芽的发育和分化。     

不同剂量锌缺乏对小鼠及其胚胎发育的影响

目的 :　用昆明种雌性小鼠建立成不同程度缺锌动物模型 ,研究不同程度锌缺乏和孕早期补锌对小鼠及其胚胎发育的影响 ,并探求其发育毒性作用的阈剂量。方法 :　实验分两阶段进行。实验一用 36只初断乳 1 4～ 1 8g小鼠 ,分为低锌 (ZD)、中锌 (ZM)、常锌 (ZN)三组 ,喂饲含锌分别为 3.0± 0 .5、1 5、30 mg/kg的饲料 ,经 50 d喂养平均体重达 30 g后交配。实验二选用 80只 ,2 5～ 30 g成熟小鼠 ,随机分为低锌组 [ZD,饲料含锌 (3.0± 0 .5) mg/kg];低锌补锌组 (ZS,于孕第 7d将低锌饲料换为含锌 30 mg/kg的常锌饲料 ) ;边缘缺锌组 (MD,饲料含锌 9mg/kg) ;常锌组(ZN,饲料含锌 30 mg/kg)。 2 5d锌耗竭性喂养后交配。所有孕鼠于妊第 1 8d活杀。结果 :　实验一 :低锌组小鼠锌水平显著低于常锌组 (P<0 .0 5) ,有典型缺锌症状 ,几乎全部出现生长抑制 ,58.33%的小鼠衰竭死亡 ,存活小鼠亦不能正常交配妊娠。 1 5mg/kg剂量组小鼠则生长发育良好 ,各项指标与常锌组间无异 (P>0 .0 5)。实验二 :ZD组小鼠血清碱性磷酸酶 (AKP)活性 ,股骨锌含量显著低于 ZN组 (P<0 .0 1 ) ;该组小鼠胚胎有明显发育不良 ,畸胎及死胎出现率显著高于 ZN组 (P<0 .0 1 )。ZS组小鼠在孕第 7d补锌后活胎仔大小已趋正常 (P>0 .0 5) ,畸胎出现率与 ZD?     

锌缺乏对脑发育的影响及机制研究

锌在生物体的生长发育中起着重要作用 ,膳食中锌缺乏可产生一系列不良后果。就孕期或哺乳期母代锌缺乏对子代脑的发育及功能影响作了概括 ,并探讨了其可能的毒性机制。     

锌缺乏对婴幼儿智能发育的影响及早期干预研究

目的:研究锌缺乏对婴幼儿智能发育的影响及早期干预的作用。方法:采用纵向追踪研究的方法,对我院系统管理中出生后1个月的足月正常婴儿进行Gesell发育诊断量表测试,从中选择600例智能发育正常的婴儿作为研究对象,于生后6个月进行末梢血微量元素锌的检测,并根据血锌水平将其分为锌缺乏组和正常对照组。在此基础上,对锌缺乏组婴幼儿进行干预性补锌3个月后,分别于生后9、12和18个月各进行1次Gesell发育诊断量表测试和末梢血微量元素锌的检测。结果:婴幼儿锌缺乏的发生率为35.50%,且锌缺乏组婴幼儿智能发育水平明显落后于正常对照组,尤其是在适应性、语言和个人社交3个能区,两者比较存在显著性差异(P<0.01)。对锌缺乏组婴幼儿进行干预性补锌后,其智能发育水平逐渐改善,9个月时两组间差异缩小,12个月时其智能发育水平与正常对照组相近,两者比较无显著性差异(P>0.05)。结论:锌缺乏将阻碍婴幼儿的智能发育,而早期干预能明显改善锌缺乏对婴幼儿智能发育的影响。     

发育期锌缺乏的行为学影响

发育期锌缺乏可引起动物食欲降低，味觉 退及周期性厌食等摄食行为的改变，亦可引起动物学习及记忆能力的下降。有关人体锌缺乏对行为学影响的研究亦有少量报道。本文就动物及人体发育期锌缺乏行为学方面的资料加以综述。     

膳食锌缺乏对发育鼠脑内NOS活性及cGMP水平的影响

一氧化氮作为一种气体性的信使分子在神经系统中参与神经细胞间的信息传递，对脑发育、学习和记忆等具有重要作用。本文研究了膳食锌缺乏对发育鼠小脑，纹状体和下丘脑中的一氧化氮合成酶（ＮＯＳ）活性和ｃＧＭＰ水平的影响，结果表明：小脑、纹状体和下丘脑中的ＮＯＳ活性和ｃＧＭＰ水平均呈发育性增高的趋势。各年龄段锌缺乏鼠小脑、纹状体和下丘脑ＮＯＳ活性均显著低于正常对照组；２１和３０日龄缺锌组仔鼠小脑、纹状体和下丘脑中的ｃＧＭＰ水平明显低于自由喂养组，锌缺乏时ＮＭＤＡ受体－ＮＯ－ｃＧＭＰ通路受损可能是锌缺乏影响脑发育和功能的一个重要机制。     

边缘性锌缺乏对大鼠肥胖的影响

目的观察边缘性锌缺乏对大鼠肥胖的影响。方法 SPF级成年雄性SD大鼠32只,随机分为4组,低锌组喂饲含6 mg/kg锌的边缘性锌缺乏饲料,中锌组喂饲含10 mg/kg锌的边缘性锌缺乏饲料,低锌对饲组和对照组喂饲正常锌含量的AIN-93M饲料。喂养6周后,处死动物。测血锌、血脂、血清瘦素含量,肝脏总抗氧化能力(T-AOC)、超氧化物歧化酶(SOD)、丙二醛(MDA)水平。结果低锌组大鼠第5周起血锌含量明显低于低锌对饲组和对照组(P0.05),成功建立边缘性缺锌模型。第6周时,低锌组大鼠脂体比明显高于低锌对饲组和对照组(P0.05);低锌组和中锌组大鼠肝脏MDA含量明显高于对照组(P0.05);低锌组和中锌组大鼠肝脏TAOC、SOD水平明显低于对照组(P0.05)。结论边缘性锌缺乏可增加肥胖发生的风险,缺锌组大鼠体内氧化应激升高可能是边缘性锌缺乏增加肥胖风险的主要原因。     

氟化物对糖尿病大鼠的毒性

用三种方法（饮水加氟，四氧嘧啶肌注，四氧嘧啶肌注和饮水加氟）处理Ｗｉｓｔａｒ大鼠，发现氟化物对糖尿病大鼠的毒性比较显著。     

硫酸镍对大鼠胚胎海马神经细胞发育毒性的研究

目的：探讨硫酸镍（NiSO4）对大鼠海马神经细胞毒作用及其机制。方法：对海马神经细胞进行原代培养，观察不同浓度的NiSO40.001、0.01、0.1、1.0、10.0、100.0μmol/L，对细胞增殖和分化的影响，并利用图像分析细胞形态的变化。结果：NiSO4明显抑制海巴神经细胞分化和发育，集落形成率明显减少，细胞体积小，拟合细胞分化和增殖抑制曲线，计算得海马神经细胞半数分化抑制浓度（ICD50）为9.5μmol/L，半数存活抑制浓度（ICV50）为35μmol/L。并显示浓度效应关系。结论：NiSO4抑制细胞分化、增殖可能是与其抑制蛋白质合成，并导致脂质过氧化有关。     

锌对同型半胱氨酸致鼠胚心脏畸形的干预

目的探讨锌元素对同型半胱氨酸致鼠胚心脏发育畸形的影响作用及可能机制。方法Sprague-Dawley(SD)成年健康清洁级雌、雄大鼠各40只,常规方法交配获取孕鼠后,随机分为5个组:1空白对照组、2同型半胱氨酸致畸组、3锌 同型半胱氨酸组、4叶酸 同型半胱氨酸组、5叶酸 锌 同型半胱氨酸组(联合组),每组8只。各组孕鼠分别于妊娠第13、15、17、19天剖腹取出胚胎,通过切片进行胎鼠心脏组织学畸形观察。结果孕周注射同型半胱氨酸后,胚胎总畸形率与空白对照组相比显著增高(χ2=53.98,P<0.01),锌 同型半胱氨酸组与同型半胱氨酸致畸组比较,畸形率明显减少(χ2=10.50,P<0.01);各妊娠天数同型半胱氨酸致畸组胚胎心脏畸形率与空白对照组相比亦显著增高(χ2分别为5.74、9.63、5.96、10.08,均P<0.01),主要畸形表现为发育延迟、心房缺如、室间隔缺损、心室缺损及大体畸形等,锌 同型半胱氨酸组与同型半胱氨酸致畸组比较,各相应天数畸形率明显减少(χ2分别为3.77、4.30、3.83、4.02,均P<0.05)。同型半胱氨酸致畸组孕鼠血清铜锌-超氧化物歧化酶活力值较对照组比较明显下降(t=8.28,P<0.01);锌 同型半胱氨酸组与同型半胱氨酸致畸组比较铜锌-超氧化物歧化酶活力值则明显增加(t=5.54,P<0.01)。结论孕周注射同型半胱氨酸对大鼠胚胎有明显致畸作用,锌元素能够有效地拮抗同型半胱氨酸的致畸作用,并且有可能是通过抑制氧化反应的发生来发挥作用的。     

Effects of biotin deficiency on embryonic development in mice

ObjectiveThe purpose of this investigation was to determine the effects of biotin deficiency on maternal metabolism and embryonic development in pregnant mouse dams.MethodsThe pregnant mice were randomly assigned to one of three dietary groups and given a biotin-deficient diet, biotin-supplemented diet, or biotin-control diet during gestation. On days of gestation (dgs) 0, 4, 8, 12, and 16, organic acids including 3-hydroxyisovaleric acid in urine were discovered by high-performance liquid chromatography, and the biotin level in the serum and urine was determined by a bioassay. On dg 18, fetuses were examined for morphologic development.ResultsIn the biotin-deficient group, biotin excretion in urine decreased on dg 4 and was subsequently below the lower limit, whereas the urinary concentration of 3-hydroxyisovaleric acid increased after dg 12. In contrast, the biotin concentration in urine significantly increased on dgs 4, 8 and 12 in the biotin-supplemented group, but decreased on dg 16 in the biotin-supplemented and biotin-control groups. The urinary excretion of pyruvic acid in the biotin-deficient group was significantly higher than that in the biotin-supplemented group throughout the entire gestation. These concentrations in urine significantly increased on dg 16 compared with dg 0. The inhibition of embryonic development and external malformations such as cleft palate (100%), micrognathia (100%), and micromelia (91.4%) were also detected in biotin-deficient fetuses.ConclusionThese findings indicated that, as the requirement of biotin increases during gestation and/or embryonic development, a large amount of biotin is necessary for maintaining normal reproductive performance during the late stage of gestation.     

Effects of marginal zinc deficiency on subclinical lead toxicity in the rat neonate

Influence of maternal dietary zinc intake on tissue distribution of lead and zinc in neonatal rats administered lead acetate by gavage during lactation was examined. Milk from dams fed a marginally deficient diet (6 micrograms Zn/g diet) contained a lower zinc concentration at the beginning of lactation than did that from control dams (30 micrograms Zn/g diet); no differences were seen by d 11 of lactation. Dams fed the deficient diet had lower plasma zinc values in comparison with pair-fed or ad libitum-fed dams and lower femur zinc concentration in comparison with pair-fed dams. Pups suckling marginally deficient dams had lower concentrations of zinc in plasma, femurs and kidneys although hippocampal and cerebellar zinc were unaltered. Body weights of pups from marginally zinc-deficient dams were lower than those from ad libitum-fed dams, but similar to those from pair-fed dams. Lead ingestion had no effect on body weight. Marginally zinc-deficient pups had greater lead accumulation in blood, femurs, hippocampi and cerebella, but not kidney, than did zinc-adequate pups. Marginal zinc deficiency during lactation increases the body lead burden of suckling rats, an effect not attributable to increased transfer of lead into milk in response to suboptimal maternal zinc status.     

Effects of dietary manganese deficiency on rat pancreatic amylase mRNA levels.

Manganese deficiency is associated with increased pancreatic amylase activity in rats. The present study investigated whether this increase in amylase activity is associated with increased pancreatic amylase messenger RNA (mRNA) levels. Weanling rats were fed a high carbohydrate diet containing either 40 micrograms Mn/g (control) or 0.5 microgram Mn/g (deficient) for 4 to 8 wk. Mn deficiency was confirmed by determining hepatic Mn content, which was significantly lower in Mn-deficient rats than in controls. Pancreatic RNA from both groups of rats was hybridized with 32P-labeled complementary DNAs for amylase and trypsinogen. Amylase mRNA levels were increased in rats fed Mn-deficient diets for both 4 wk (200%) and 8 wk (250%) when compared with respective control levels. In contrast, Mn deficiency was not associated with alterations in trypsinogen mRNA levels. Serum levels of insulin and corticosterone, hormones known to increase pancreatic amylase mRNA, were not affected by Mn deficiency. These observations suggest that Mn may participate in the regulation of amylase gene expression in a manner that is independent of insulin and corticosterone.     

Effects of vitamin A deficiency on mitochondrial function in rat liver and heart

The aim of this study was to investigate comparative effects of vitamin A deficiency on respiratory activity and structural integrity in liver and heart mitochondria. Male rats were fed a liquid control diet (control rats) or a liquid vitamin A-deficient diet (vitamin A-deficient rats) for 50 days. One group of vitamin-A deficient rats was refed a control diet for 15 days (vitamin A-recovered rats). To assess the respiratory function of mitochondria the contents of coenzyme Q (ubiquinone, CoQ), cytochrome c and the activities of the whole electron transport chain and of each of its respiratory complexes were evaluated. Chronic vitamin A deficiency promoted a significant increase in the endogenous coenzyme Q content in liver and heart mitochondria when compared with control values. Vitamin A deficiency induced a decrease in the activity of complex I (NADH-CoQ reductase) and complex II (succinate-CoQ reductase) and in the levels of complex I and cytochrome c in heart mitochondria. However, NADH and succinate oxidation rates were maintained at the control levels due to an increase in the CoQ content in accordance with the kinetic behaviour of CoQ as an homogeneous pool. On the contrary, the high CoQ content did not affect the electron-transfer rate in liver mitochondria, whose integrity was preserved from the deleterious effects of the vitamin A deficiency. Ultrastructural assessment of liver and heart showed that vitamin A deficiency did not induce appreciable alterations in the morphology of their mitochondria. After refeeding the control diet, serum retinol, liver and heart CoQ content and the activity of complex I and complex II in heart mitochondria returned to normality. However, the activities of both whole electron transfer chain and complex I in liver were increased over the control values. The interrelationships between physiological antioxidants in biological membranes and the beneficial effects of their administration in mitochondrial diseases are discussed.     

Reevaluation of zinc deficiency on concanavalin-A-induced rat spleen lymphocyte proliferation

Zinc concentrations of serum, nonlymphoid and lymphoid tissues, and the responsiveness of concanavalin-A (Con-A)-stimulated spleen lymphocytes (SL) and cervical lymph node cells ( CLNC ) from ad libitum-fed zinc-deficient (ZD), pair-fed (PF) and ad libitum-fed zinc-adequate rats (AL) were determined. In vitro effects of serum from ZD, PF and AL rats on responsiveness of Con-A-stimulated SL and CLNC were determined. Weanling male Long-Evans rats were fed ad libitum zinc-deficient (less than 1.0 microgram Zn/g diet) and zinc-adequate (20 micrograms Zn/g diet) diets for 7-42 days. Effects of undernutrition on test parameters were determined on PF rats, which received a restricted zinc-adequate diet (restricted in amount to that consumed by ZD rats). Growth, food intake and zinc concentrations in serum, liver and pancreas were significantly depressed in ZD and PF rats. Zinc per gram of thymus tissue and per number of SL was elevated in ZD and PF rats. Spleen lymphocytes from ZD and PF rats displayed equivalent to significantly increased levels of proliferation following stimulation with Con-A. [3H]Thymidine incorporation by Con-A-stimulated SL and CLNC from ZD, PF and AL rats was not significantly different when cultured in medium containing serum from ZD, PF and AL rats. The present study shows that zinc deficiency causes major changes in total-body and organ growth but minor changes in zinc content and mitogen-induced proliferation of lymphocytes.     

化学因素对胚胎发育的影响

胚胎发育是非常复杂而且变化极为协调的生理过程.在此过程中,外界环境中多种因素的影响都可能导致胚胎死亡或是胎儿畸形.随着环境污染日趋加重,环境因素对胚胎发育的影响也受到人类的日趋重视.影响胚胎发育的因素可分为物理、化学和生物三大类.它们对胚胎发育的作用及其可能机制尚未完全明了.该文主要就化学因素对胚胎发育的影响及其机制进行综述.