缺锌对大鼠血液皮质醇和ACTH含量及大脑皮质NO合酶活性的影响

就缺锌对大鼠血液皮质醇和促肾上腺皮质激素（ACTH）含量以及大脑皮质NO合酶活性的影响进行了研究,生长大鼠随机分为3组,即缺锌组,对喂组和缺锌补锌组（先饲喂缺锌饲料21天后再补锌）,饲养实验的持续时间为35d。与对喂组比较,缺锌组大鼠血液中皮质醇含量显著升高,而血液ACTH浓度以及大脑皮质NO合酶活性明显降低,此结果提示锌可影响下丘脑－垂体一肾上腺皮质轴和NO合酶的代谢。     

水母雪莲细胞培养物调血脂作用的初步研究

为研究水母雪莲细胞培养物对高脂大鼠的调血脂作用,将雄性SD大鼠分为4组：正常对照组(A组)、高脂模型组(B组)、高剂量组(C组)和低剂量组(D组)。A组喂基础饲料,B组喂高脂饲料,C组喂高脂饲料的同时饲以大剂量水母雪莲细胞培养物,D组喂高脂饲料的同时饲以小剂量水母雪莲细胞培养物。给药1/d,3周后采血,测定血脂水平及肝肾功能。C组较B组各项血脂指标均有改善,各组间肝肾功能未见显性差异。初步研究表明,水母雪莲细胞培养物对高脂大鼠具有调血脂的作用。本实验用药剂量安全。     

饲料中添加不同含量的微量元素锌对河蟹雄性生殖腺的影响

通过投喂不同锌含量的人工配合饲料,研究饵料微量元素锌对雄性中华绒螯蟹性腺发育的影响。以ZnSO4为锌源,对照组投喂未添加锌的基础饲料,实验1组至实验4组分别投喂:添加50mg/kg饲料、100mg/kg饲料、200mg/kg饲料、400mg/kg饲料的配合饲料。实验为期70d,结果如下:精巢和副性腺锌含量均以实验2组最高,分别为300mg/kg和150mg/kg,对照组分别为85mg/kg和67mg/kg。睾酮含量和性腺指数亦以实验2组最高,分别为0.835ng/mL和25.94×10-3。精巢碱性磷酸酶和乳酸脱氢酶活性在整个实验过程中呈现先上升后下降的趋势,以30d时达到最高,而同一时间各组间的活性均以实验2组最高。副性腺碱性磷酸酶和乳酸脱氢酶活性分别在50d和70d时出现两个峰值,而同一时间各组间酶活性均以实验2组最高,其中碱性磷酸酶在达到峰值后急剧下降,实验结束时活性极低。结果表明:随着饵料锌含量的增加,河蟹生殖器官内锌的积累量也逐渐上升,但若超出最适添加量,则积累量反而下降。饵料中适量添加锌可促进河蟹生殖器官的发育和睾酮的分泌,河蟹精巢和副性腺中乳酸脱氢酶和碱性磷酸酶的活性明显与其锌含量相关。     

饲料能量密度和投喂水平对吉富罗非鱼生长和健康的影响

为探讨饲料能量密度(DED)和投喂水平(DFR)对鱼类生长和健康的影响,本试验采用2×2双因子设计,设置2个DED(对照组和高糖高脂组)和2个DFR(1倍和1.2倍表观饱食投喂对照组饲料的能量水平),研究DED和DFR对吉富罗非鱼[Oreochromis niloticus,(14.59±0.06)g]生长性能、饲料利...     

小麦种子含锌量在幼苗中的分配与对缺锌敏感性的关系

应用三个种子含锌量不同的小麦品系为实验材料,研究了在缺锌和供锌条件下锌在小麦幼苗中的分配规律。实验证明在缺锌的条件下,小麦幼苗植株含锌量与种子的含锌量成正相关。锌在三个品系小麦不同叶位中的分配规律是一致的,但种子含锌量低的小麦向幼叶中分配的锌量比例大。在供锌的条件下,种子含锌量高的品系地上部的总锌量比低锌品系高。     

小麦种子含锌量在幼苗中的分配与对缺锌敏感性的关系

应用三个种子含锌量不同的小麦品系为实验材料,研究了在缺锌和供锌条件下锌在小麦幼苗中的分配规律。实验证明在缺锌的条件下,小麦幼苗植株含锌量与种子的含锌量成正相关。锌在三个品系小麦不同叶位中的分配规律是一致的,但种子含锌量低的小麦向幼叶中分配的锌量比例大。在供锌的条件下,种子含锌量高的品系地上部的总锌量比低锌品系高。     

不同苹果砧木对缺锌胁迫的耐性评价

为筛选适应缺锌胁迫环境的砧木资源,以山定子、丽江山定子、小金海棠、锡金海棠、新疆野苹果、八棱海棠、平邑甜茶、火焰海棠8种苹果砧木资源为试材,对砧木株高、干物质量、根系构型及锌含量等指标进行测定,利用模糊隶属函数法进行耐缺锌能力综合评价.结果表明： 缺锌处理下,丽江山定子、锡金海棠和新疆野苹果均先表现出新生叶小、簇生等缺锌症状,而小金海棠、火焰海棠缺锌症状不明显;缺锌显著降低了苹果砧木株高和地上部锌积累量,而小金海棠的降低幅度最小;缺锌胁迫下小金海棠和山定子叶片锌含量较高,分别为23.2和21.3 mg·kg^-1.采用模糊隶属函数法综合评价参试砧木耐缺锌能力：小金海棠最强,火焰海棠次之,山定子、锡金海棠、八棱海棠和平邑甜茶的耐缺锌能力较弱,丽江山定子和新疆野苹果的耐缺锌能力最弱.     

低锌和缺锌对玉米生长发育的影响

以玉米沈单10号为材料,用溶液培养的方法研究了缺锌、低锌和正常供锌对玉米生长发育的影响,进一步明确了一定量低锌比缺锌对玉米的伤害更大,并对其POD、SOD、CAT同工酶谱及蛋白质表达进行了分析、结果表明：一定浓度的低锌培养使玉米生长受抑及受害最重,且地上部分比地下部分更敏感。低锌和缺锌处理时3种同工酶的酶谱和蛋白表达与正常供锌时均有明显的差异,尤其在一定量低锌浓度时,有些同工酶的表达增强或被特异性诱导,而另一些酶的合成受阻;低锌和缺锌处理都诱导出了新的蛋白组分,也缺失了部分蛋白组分,且低锌比缺锌时缺失的蛋白组分更多。这些变化可能与玉米生长发育及受害密切相关。     

降胆固醇益生菌联合大豆卵磷脂辅助降血脂保健食品的功能评价

目的研究降胆固醇益生菌联合大豆卵磷脂的保健食品的辅助降血脂作用。方法雄性SD大鼠喂普通饲料7d后,根据血清总胆固醇(TC)水平随机分成5组,每组10只,分别为样品高、中、低3个剂量组,模型对照组和空白对照组。以灌胃方式(10mL/kg)给予受试物,除空白对照组外,各组均喂高脂饲料,连续喂养30d后,称重、取大鼠眼血测定各项血脂指标。结果样品的低、中、高剂量组均能使高胆固醇血症大鼠血清TC和低密度脂蛋白胆固醇(LDL-C)水平降低,与模型对照组比较差异有统计学意义(P0.05)。结论降胆固醇益生菌联合大豆卵磷脂的保健食品对大鼠具有辅助降血脂作用。     

丙氨酰-谷氨酰胺投喂方式对建鲤生长、抗氧化及免疫力的影响

以初始质量为(33.52±0.17)g建鲤鱼种为研究对象,在室内单循环养殖系统中进行8周(w)生长试验,分别配制添加0.0%(对照饲料)和0.5%(试验饲料)丙氨酰-谷氨酰胺(Ala-Gln)的等氮(35 g/kg粗蛋白)、等能(17kJ/g能量)饲料,采用5种不同的Ala-Gln投喂方式[连续8w投喂对照饲料(I,对照组);试验饲料2w交替投喂(II);前4w投喂试验饲料、后4w投喂对照饲料(III);前4w投喂对照饲料、后4w投喂试验饲料(IV);8w连续投喂试验饲料(V)],探讨Ala-Gln投喂方式对建鲤生长、抗氧化及免疫力的影响。结果表明:Ala-Gln连续投喂和不连续投喂的生长都显著高于对照组(P<0.05)。2w交替投喂的生长率显著高于4w交替和连续8w投喂试验饲料组(P<0.05),前4w投喂试验饲料且后4w投喂对照饲料的生长率要高于8w连续投喂试验饲料组(P<0.05)。后4w投喂试验饲料组和连续8w投喂试验饲料组的血清SOD显著高于对照组(P<0.05);连续8w投喂试验饲料组显著高于2w交替投喂试验饲料组和前4w投喂试验饲料组的血清SOD(P<0.05)。Ala-Gln各种投喂方式组的肝胰脏谷胱甘肽过氧化物酶(GSH-Px)都显著高于对照组(P<0.05)。后4w投喂试验饲料组和连续8w投喂试验饲料组的血清GSH-Px显著高于对照组(P<0.05)。在Ala-Gln四种投喂方式组中,除2w交替投喂组外,其他三种投喂方式组的头肾LZM都显著高于对照组(P<0.05)。后4w投喂试验饲料组和8w连续投喂试验饲料组的脾脏LZM都显著高于对照组(P<0.05)。对照组头肾NO要显著高于各投喂方式组(P<0.05)。在试验条件下,饲料中添加Ala-Gln可提高建鲤的生长、抗氧化和免疫力。不同投喂方式间亦有显著差异,从生长、抗氧化和免疫的角度,结合经济性和适用性等进行考虑,建议采用2w间隔投喂的方式。     

Maternal zinc deficiency impairs brain nestin expression in prenatal and postnatal mice

INTRODUCTIONZinc is essential for normal brain development,evidenced by the fact that zinc deficiency in lactating mothers is characterized by a high incidence ofneuroanatomical maiformatinns and functional abnormalities in suckling offspring[1-3]. By colltrast,relatively little is known about the relationship be{tween maternal zinc nutrition and fetal brain development[2, 4, 5]. Dvergsten et al[6-81 investigated theeffects of maternal zinc deficiency on postnatal development of the rat ce…     

Developmentally regulated expression of specific tau sequences

Tau protein undergoes a shift in its molecular mass and its electrophoretic complexity during early postnatal development. We have sequenced a tau cDNA from an adult rat brain expression library and have found two inserted sequences. One of these inserts predicts a fourth repeated sequence homologous to the other three in the carboxyl end of tau that have the property of microtubule binding. Oligonucleotide probes directed against the insert hybridized only to tau mRNA at postnatal time points, even though tau is first expressed as early as embryonic day 13. A probe directed against the junction revealed expression of non-insert-containing tau mRNA from embryonic day 14 until postnatal day 8, after which time there was an abrupt decline in the expression of this immature form. Comparison of the developmentally expressed tau sequences with those sequences obtained directly from Alzheimer paired helical filaments revealed the presence of both the mature and the immature tau mRNA sequences.     

The ontogeny and phylogenetic conservation of MAP 2 forms

Summary In the adult rat brain, MAP 2 is a high-molecular weight protein that is highly concentrated in dendrites. Immunoblots of homogenates of developing rat brain have indicated that a low-molecular weight form of MAP 2, MAP 2 c, is transiently expressed as the brain is undergoing morphogenesis. Using MAP 2-specific monoclonal antibodies, we have demonstrated that the compartmentalization of high-molecular weight MAP 2 and the developmental regulation of MAP 2 are conserved in mammalian, avian, and amphibian brain. We have also determined the distribution of MAP 2 c in developing neuronal tissue. MAP 2 c appears before high-molecular weight MAP 2 in developing neurons, and in contrast to the dendrite-specific high-molecular weight forms of MAP 2, MAP 2 c is present in axons and glia. We have also shown that MAP 2 c is present in the adult rat retina, where it is concentrated in regenerative photosensitive cells. The transient expression of MAP 2 c in the developing brain of three species as well as in adult photosensitive cells suggests a role for this protein in neurite growth and plasticity.Abbreviations MAP microtubule-associated protein - E embryonic day - P postnatal day     

Maternal zinc deficiency reduces NMDA receptor expression in neonatal rat brain, which persists into early adulthood

Prenatal and early postnatal zinc deficiency impairs learning and memory and these deficits persist into adulthood. A key modulator in this process may be the NMDA receptor; however, effects of zinc deficiency on the regulation of NMDA receptor activity are not well understood. Female Sprague-Dawley rats were fed diets containing 7 (zinc deficient, ZD), 10 (marginally zinc deficient, MZD) or 25 (control) mg Zn/g diet preconception through postnatal day (PN) 20, at which time pups were weaned onto their maternal or control diet. Regulation of NMDA receptor expression was examined at PN2, PN11, and PN65. At PN2, expression of whole brain NMDA receptor subunits NR1, NR2A, and NR2B was lower in pups from dams fed ZD and MZD compared to controls, as analyzed using relative RT-PCR and immunoblotting. At PN11, whole brain and hippocampi NR1, NR2A, NR2B and PSA-NCAM (polysialic acid-neural cell adhesion molecule) expression and the number of PSA-NCAM immunoreactive cells were lower in pups from dams fed ZD compared to controls. Whole brain brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) concentrations were lower in pups from dams fed ZD or both low zinc diets, respectively. Whole brain NR1 expression remained lower in previously zinc-deficient rats at PN65. These data indicate potential mechanisms through which developmental zinc deficiency can impair learning and memory later in life.     

Influence of maternal dietary zinc intake on in vitro tubulin polymerization in fetal rat brain

The hypothesis that one of the biochemical lesions underlying zinc deficiency-induced teratogenicity is altered microtubule formation was tested. Day 19 fetuses from zinc-deficient Sprague-Dawley dams were characterized by low brain supernate zinc concentrations and slow brain tubulin polymerization rates compared to controls. Brain supernate tubulin and protein concentrations were similar in zinc-deficient and control fetuses. In vitro brain tubulin polymerization rates were increased following addition of zinc to either control or zinc-deficient brain supernates; however, the stimulatory effect of added zinc on polymerization was significantly higher in brain supernates obtained from zinc-deficient fetuses compared to controls. These results support the idea that one effect of fetal zinc deficiency is a reduction in tubulin polymerization, which in turn may result in altered microtubule function.     

微管相关蛋白tau在不同年龄大鼠海马内的定位分布特点

目的 检测微管相关蛋白tau和Ser396/404位点磷酸化tau在胚胎期大鼠和出生后直至成熟期大鼠海马内的表达及变化规律,浅析与神经细胞分裂和分化的关系.方法 用免疫组织化学SABC法显示孕18d、出生后1d、1w、2w、2m的大鼠脑冠状切面总tau（R134d）、Ser396/404位点磷酸化tau（PHF-1）的表达.结果 ①胚胎期大鼠海马CA区的锥体细胞数量明显多于出生后,随着脑的发育,锥体细胞层的神经细胞数量逐渐下降;②孕18d大鼠海马内有丰富的总tau和PHF-1 tau的表达,并且海马内各区的阳性物质表达均匀,生后1d和1w两种物质表达仍然很强,阳性产物主要分布在海马CA1和CA2区以锥体细胞轴突为主要成分的始层,在锥体细胞树突集中的分子层和胞核内也有少量分布,而在生后2w和2m大鼠海马内各区均未见密集的阳性产物表达.结论 不同年龄大鼠海马内总tau和PHF-1 tau的表达和分布变化可能与神经系统发育过程中细胞的分裂和分化有关.     

Effects of marginal zinc deficiency on microtubule polymerization in the developing rat brain

One of the possible mechanisms that has been proposed to underlie the deleterious effects of zinc deficiency on brain development is an impairment in the normal formation of the cytoskeletal network. In the current study, in vivo microtubule polymerization was characterized in brain supernatant fluids, from 20-d-old pups whose dams were fed diets containing control (50 micrograms zinc/g) or marginal levels of zinc (10 micrograms zinc/g) throughout pregnancy and lactation. Pup brain and body weights were similar between the groups; however, plasma zinc concentrations were lower (27%) in pups fed the marginal zinc diet than in controls. Tubulin concentrations in 100,000 g brain supernates were similar between the groups; however, tubulin polymerization in the brain supernates was significantly lower in pups fed the marginal zinc diet compared to controls. Primarily, the early events of polymerization were affected; the lag period of the reaction was doubled, and the initial velocity was slower (26%) in supernates from pups fed the marginal zinc diet than in controls. These findings support the idea that some of the negative effects of marginal zinc deficiency on brain development and function may be mediated by an alteration in microtubule formation.     

The effect of late prenatal and/or early postnatal zinc deficiency on the development and some biochemical aspects of the cerebellum and hippocampus in rats

In rats, late prenatal and/or early postnatal zinc deficiency results in behavioural anomalies in adult animals, but not in overt dysmorphogenesis of the central nervous system. Cerebellar and hippocampal development occurs mainly in the first three weeks postnatally and zinc accumulates specifically in the mossy fibres of the hippocampus during this period.In the present investigation, rat pups were suckled by dams fed a zinc-deficient (<0.5 mg/kg) diet either from day 19 of pregnancy or from parturition. Control animals were restricted-fed the same diet supplemented with 100 mg zinc/kg. Studies were performed on pups either on day 18 postpartum in the case of animals fed the experimental diets from parturition, or on day 20 for pups which received treatment from day 19 of gestation.Cerebellar and hippocampal weights were lower in pups suckling from zinc-deficient dams but zinc levels were not affected in either organ, although histological evidence suggested less zinc in the hippocampal mossy fibres. Incorporation of H-thymidine into cerebellar and hippocampal DNA was not affected by maternal zinc status, nor was the activity of the zinc metalloenzyme alkaline phosphatase.The activity of the myelin-marker enzyme 2′, 3′-cyclic nucleotide 3′-phosphohydrolase was substantially lower in both regions of the brain in zinc deprived pups, especially in the hippocampus. Activity of the zinc metalloenzyme L-glutamic acid dehydrogenase was also diminished in both tissues from 20-day-old pups and in the hippocampi of 18-day-old animals.The data suggest that cerebellar and hippocampal DNA synthesis is not seriously affected by late prenatal and/or early postnatal zinc depletion, but that the activities of two enzymes associated with neural function are. The possibility is raised that these defects may be associated with the behavioural changes observed in rats subjected to zinc impoverishment during the period of maximal cerebellar and the hippocampal development.     

Early-in-life dietary zinc deficiency and supplementation and mammary tumor development in adulthood female rats

Zinc deficiency during pregnancy and postnatal life can adversely increase risk of developing human diseases at adulthood. The present study was designed to evaluate whether dietary zinc deficiency or supplementation during the pregnancy, lactation and juvenile stages interferes in the development of mammary tumors induced by 7,12-dimethylbenzanthracene (DMBA) in female Sprague–Dawley (SD) rats. Pregnant female SD rats were allocated into three groups: zinc-adequate diet (ZnA - 35-mg/kg chow), zinc-deficient diet (ZnD - 3-mg/kg chow) or zinc-supplemented diet (ZnS - 180-mg/kg chow) during gestational day 10 (GD 10) until the litters' weaning. Female offspring received the same diets as their dams until postnatal day (PND) 51. At PND 51, the animals received a single dose of DMBA (50 mg/kg, ig) and zinc-adequate diets. At PND 180, female were euthanized, and tumor samples were processed for histological evaluation and gene expression microarray analysis. The ZnD induced a significant reduction in female offspring body weight evolution and in mammary gland development. At late in life, the ZnD or ZnS did not alter the latency, incidence, multiplicity, volume or histological types of mammary tumors in relation to the ZnA group. However, the total tumor number in ZnS group was higher than in ZnA group, accompanied by distinct expression of 4 genes up- and 15 genes down-regulated. The present findings indicate that early-in-life dietary zinc supplementation, differently to zinc deficiency, has a potential to modify the susceptibility to the development of mammary tumors induced by DMBA.     

Developmental regulation of two microtubule-associated proteins (MAP2 and MAP5) in the embryonic avian retina

Previous studies with the mammalian brain have shown that the expression of a number of neuronal microtubule-associated proteins (MAPs) is developmentally regulated. For example, the low-molecular-weight form of MAP2 (MAP2c) is abundant in neonatal rat brains and is less abundant in adults. Similarly, MAP5 levels decrease during postnatal development. Using monoclonal antibodies, we have followed the time of first appearance, cellular distribution, and molecular form of MAP2 and MAP5 during the morphogenesis of the quail retina. MAP2 first appears in ganglion cell bodies and in the axons of the optic fibre layer (OFL) at embryonic day 4 (E4). Anti-MAP2 staining remains restricted to these sites until E10, when staining appears in the inner plexiform layer (IPL). At E14, one day before hatching, anti-MAP2 staining is found in three broad laminae in the IPL, as well as in photosensitive cells. MAP5 is present in ganglion cell axons from the onset of neurite elongation at E3 and is limited to the OFL until E10. The intensity of anti-MAP5 staining in the OFL and optic nerve decreases after E7, which corresponds with a decrease in the number of actively growing ganglion cell axons. By E14, anti-MAP5 stains five layers in the IPL that correspond with layers of amacrine cell process arborizations. Western blots of E10 brain microtubule proteins show that MAP2 is represented by both a 260 x 10(3) Mr protein and a 60-65 x 10(3) Mr protein; the latter is much more abundant. Anti-MAP5 recognizes a 320 x 10(3) Mr brain microtubule protein in both the quail and the rat. We conclude that the cellular distribution, developmental regulation and molecular forms of MAP2 and MAP5 are similar in the rat and quail, suggesting that these molecules have conserved and hence fundamental roles in the growth and differentiation of neuronal processes.