长期有氧运动和饮食铁含量对雌性大鼠血液铁和海马贮存铁的影响

目的观察饮食铁含量和长期有氧运动对雌性大鼠血液铁状态和海马非血红素铁（NHI）贮存的影响,探讨外周铁浓度与脑铁浓度的变化关系。方法采用断乳雌性SD大鼠71只,随机分为3组：饮食低铁含量组（12mg／kg）,饮食标准铁含量组（45mg／kg）和饮食高铁含量组（1000mg／kg）,其中每一组再分为运动组和静息组。用相应的铁含量饲料喂养1个月后,运动组进入游泳期,每周5d,每天1次,每次30min,持续3个月。静息组除不进行运动外,其余处理与对应运动组相同。在末次运动后,所有大鼠禁食24h,用戊巴比妥钠麻醉后静脉取血,测定红细胞相关指标和血清铁状态指标;断头取全脑,冰上快速分离出海马,测定海马NHI含量。结果与标准铁含量静息组比,低铁含量静息组血红蛋白（Hb）、红细胞压积（HCT）、平均红细胞体积（MCV）和平均红细胞血红蛋白量（MCH）均降低（P〈0．05）,红细胞分布宽度（RDW）和血浆总铁结合力（TIBC）升高（P〈0．05）。低铁含量饮食时（ID）,与静息组比,运动组Hb、HCT显著升高（P〈0．01）,海马NHI含量升高（P〈0．05）,血清铁（SI）、转铁蛋白饱和度（TS）均显著降低（P〈0．01）。高铁含量饮食时（SU）,与静息组比,运动组血浆TIBC升高（P〈0．05）,TS降低（P〈0．05）。结论低铁含量饮食导致雌性大鼠出现血液低铁状态,机体对于饮食铁不足有适应性调节;低铁饮食下长期低强度运动会加重雌性大鼠血液低铁状态,并且导致脑内海马铁贮存水平升高。     

铝染毒对大鼠海马中五种元素含量的影响

目的　探讨铝染毒后对大鼠海马中的锌、铁、铜、钙元素的含量的影响。方法　按大鼠体重 8%的进食量计算 ,分别在基础饲料中添加AlCl3·6H2 O ,分别按 0 (A) ,1 1 2 (B) ,55 9(C) ,1 1 1 9(D)mgAl3+ /kgBW 4个剂量组连续喂饲SD雄性大鼠 90d。然后 ,用原子吸收分光光度法测定大鼠海马中铝、锌、铁、铜和钙的含量。结果　铝经口染毒后 ,大鼠海马中铝含量明显升高 ,且有显著的剂量效应关系。对照组与 3个铝染毒剂量组脑海马中锌、铁、钙、铜含量分别为 :A组 (1 8 2 9± 2 48,2 4 86±1 97,48 69± 2 2 0 8,4 53± 0 99) μg/g ;B组 (1 7 2 2± 2 0 6 ,2 7 54± 2 87,42 79± 1 4 42 ,4 0 6± 0 41 ) μg/g ;C组 (1 4 46± 1 90 ,2 0 1 8± 2 79,2 9 95± 7 33 ,3 98± 0 2 5) μg/g;D组 (1 5 85± 2 54 ,2 0 96± 2 83 ,36 1 4± 1 2 66 ,4 53± 0 58) μg/g。与对照组比较 ,B、C组锌、铁含量均有显著性降低 ,C组的钙有显著性降低。结论　铝经口染毒会造成铝在脑海马中蓄积 ,并对其他一些必需元素在脑海马中的含量产生不同程度影响     

长期摄铝对大鼠海马铝、铁、锌含量和脂质过氧化的影响

为研究长期摄铝对大鼠海马铝、铁、锌、铜含量和脂质过氧化的影响 ,进一步探明铝的神经毒作用机理 ,选择雄性SD大鼠 ,按体重随机分为对照组和 3个实验组 (低铝、中铝、高铝组 ) ,实验组在基础饲料中添加氯化铝 ,使Al3+ 剂量分别为 11 2、5 5 9和 111 9mg kgBW ,连续染毒 90天。采用旷场行为实验和被动回避实验观察神经行为学改变 ;原子吸收法测定铝、铁、锌、铜含量 ;分光光度法测定超氧化物歧化酶 (SOD)和谷胱甘肽过氧化物酶 (GSH Px)活性及丙二醛 (MDA)含量。结果显示 :与对照组比较 ,实验组大鼠自发活动能力下降 ,被动回避潜伏期缩短 ;大鼠海马铝含量升高 ,铁、锌含量下降 ;SOD和GSH Px活性下降 ,MDA含量升高。提示长期摄铝可致大鼠海马铝富集并干扰铁、锌的正常分布 ,抗氧化酶活性降低 ,脂质过氧化水平升高。海马富集铝以及铁、锌含量的变化和海马氧化损伤可能是导致铝的神经毒性的重要原因之一。     

高锌饮食对大鼠海马超微结构的影响

给鼠饲以添加不同含量的高锌饲料，分别于每ｋｇ干饲料中加硫酸锌２００（Ｚ１组），４００（Ｚ２组），８００（Ｚ３组），１２００（Ｚ４组）ｍｇ／ｋｇ。历时１２周观察其海马的形态学变化。结果显示：①光镜下海马结构无明显改变。②电镜下Ｚ１组、Ｚ２组海马结构基本正常。Ｚ３、Ｚ４组神经元内线粒体内部嵴断裂，基质淡化，严重者呈空泡变性，溶酶体增多，髓鞘融合，突触数量明显减少。提示服用过高剂量锌可引起海马超微结构的改变，从而影响脑功能。     

多氯联苯对雄性大鼠海马神经元棘密度及bcl-2表达的影响

为探讨多氯联苯(polychlorinated biphenyl PCB)对大鼠海马组织结构和功能的影响,进一步认识PCB致海马损伤的机制。将45只雄性Wistar大鼠随机分为4组。对照组(9只)饲喂正常饲料,低、中、高剂量组(各12只)分别饲喂不同PCB含量的颗粒饲料(0.1、1、10mg/kg)染毒3个月后,利用Golgi镀银染色技术、免疫组织化学方法,研究PCB对大鼠海马锥体细胞棘密度及B细胞淋巴瘤因子2(B-cell lymphoma2,bcl-2)表达的影响。结果显示随着PCB剂量的增加大鼠海马锥体细胞神经元基树突及侧树突棘发育受损,中、高剂量组海马锥体细胞基树突及侧树突棘密度同对照组相比显著降低(P0.01);低、中剂量PCB能促进海马神经组织bcl-2表达(P0.01),高剂量PCB组bcl-2表达显著下调。结果提示,本研究剂量的PCB能影响大鼠海马神经元棘密度及bcl-2表达。     

1800 MHz电磁辐射对雄性大鼠海马感觉门控P50的影响

目的 探讨1 800 MHz电磁辐射对雄性大鼠海马感觉门控P50的影响,为移动通讯技术可能引起的健康危害提供实验依据.方法 将48只4周龄SPF级SD雄性大鼠按体重随机分为4组,每组12只.暴露组用1 800MHz射频电磁辐射对大鼠进行21 d连续暴露,每天12 h,功率密度分别为0.5(暴露I组)和1.0mW/cm2(暴露Ⅱ组),同时设置对照组.采用条件-试验双声刺激模式记录海马感觉门控P50,通过比较暴露组与对照组听觉诱发电位的差异.识别1 800 MHz电磁辐射对大鼠海马感觉门控P50的影响.结果 暴露I组雄鼠的海马感觉门控P50的S2/S1比值和S2峰-峰值大于对照组和暴露Ⅱ组(P<0.05);其他各组间的海马感觉门控P50的S2/S1比值、S2峰-峰值、S1峰-峰值差异无统计学意义(P>0.05).结论 在本实验条件下,1 800 MHz射频波以0.5 mW/cm2的功率密度辐射对雄性大鼠海马感觉门控P50产生影响.     

铝对大鼠海马氨基酸类神经递质含量的影响

目的 从海马氨基酸类神经递质的角度,探讨铝的神经毒作用机制。方法 选择雄性SD大鼠,按体重随机分4组,在基础饲料中添加氧化铝,Al^3 剂量分别为0、11.2、55.9和111.9mg/kg体重,连续染毒90d。采用旷场行为和被动回避实验观察神经行为学改变,高效液相色谱法测定海马氨基酸类神经递质含量,原子吸收法测海马铝含量。结果 与给铝盐前比较,大鼠自发活动能力下降,被动回避潜伏期缩短。与对照组比较,Al^3 111.9mg/kg体重组海马天门冬氨酸、谷氨酰胺含量显升高,Al^3 55.9和111.9mg/kg体重组牛磺酸含量显升高,并均与染毒剂量呈明显正相关;各剂量组铝含量均显升高,并与染毒剂量呈明显正相关。结论 海马氨基酸类神经递质含量的改变可能是铝神经毒性的重要机制之一。     

铅对大鼠海马生长抑素的影响

探讨铅对大鼠海马生长抑素含量的影响以及停止接触后生长抑素的恢复情况。随着铅染毒剂量增加，血铅及皮层铅浓度均增加，海马中生长抑素含量减少；停止接触３０、９０天后，生长抑素可恢复至正常水平。     

规律运动对慢性心理应激大鼠海马锥体细胞形态的影响

目的探讨规律运动对慢性心理应激大鼠海马锥体细胞形态的影响。方法建立慢性心理应激模型结合6周游泳训练后,采用HE染色和透射电镜技术观察海马锥体细胞形态和结构变化。结果应激组大鼠海马CA3区锥体细胞胞浆凝固、胞核固缩、染色质边集,核膜皱褶,核内外可见空泡变性,线粒体变性、嵴数量明显减少,粗面内质网模糊不清、网腔局部扩张;30min运动组与对照组相似,60min运动组较对照组轻度改变,应激+30min运动组变化介于对照组和应激组之间;应激+60min运动组与应激组相似。结论心理应激导致大鼠海马CA3区锥体细胞形态和超微结构改变,适量运动调节可减缓慢性心理应激引起的损伤,对海马锥体细胞有保护作用。     

氯化镧对大鼠全血中铁、铜和锌含量的影响

随着稀土元素应用的日益广泛，越来越多的稀土进入生活环境，进入食物链。通常人或动物的稀土摄入是经消化道进入血液。血液中的各种蛋白可能成为稀土离子的配体。从而影响血液中其它微量元素的运输。为探讨饮食中稀土元素摄入对血液中微量元素平衡的影响，我们在大鼠的饮水中加入不同剂量的氯化镧。X-射线荧光法测定大鼠血液中Fe、Cu和Zn的含量，并对实验结果进行统计分析，报告如下。     

Impact of aerobic exercise on neurobehavioral outcomes

Numerous studies have examined the relationship between physical activity and cognitive function, demonstrating that greater physical activity is associated with lower incidence of cognitive impairment in later life. Due to an increasingly large number of older adults at risk for cognitive impairment, the relationship between physical activity and cognition has garnered increasing public health relevance and multiple randomized trials have demonstrated that exercise interventions among sedentary adults improve cognitive performance in multiple domains of function. This article will examine the relationship between physical activity and cognitive function by reviewing several different areas of literature, including the prevalence of cognitive impairment, assessment methods, observational studies examining physical activity and cognition, and intervention studies. The present review is intended to provide a historical tutorial of existing literature linking physical activity, exercise, and cognitive function among both healthy and clinical populations.     

Interactions of iron deficiency and exercise training in male Sprague-Dawley rats: ferrokinetics and hematology

Ferrokinetic and hematologic studies were performed using adult male Sprague-Dawley rats to determine if 12 wk of exercise training alters the delivery of iron to the red blood cell (RBC) mass, the severity of the anemia or the maximal exercise performance of moderately iron-deficient animals. Forty rats were assigned to either iron-deficient (ID) or control (CN) diets, and further subdivided into sedentary (SD) and exercised (EX) groups. Exercised groups were trained on a treadmill, at a 15% grade, 65% VO2max, for 90 min/d, 4 d/wk. After 12 wk of exercise training and dietary iron deficiency, the final body weight of IDEX rats was 90.5% that of IDSD rats. Fractional plasma iron clearance in IDEX rats was 86% of that in IDSD rats (3.32 vs. 2.85%/min). Exercise training failed to increase absolute VO2max (ml/min) or change hemoglobin concentration in iron-deficient rats. Resting oxygen consumption in IDEX rats was 116% that in IDSD rats (42.8 vs. 32.5 ml.kg-1.min-1, P less than 0.05). We conclude that exercise training and iron deficiency interact to alter iron physiology in exercised, iron-deficient animals. This interaction affects the kinetic behavior of plasma iron, growth and basal oxygen consumption.     

Effects of exercise on iron metabolism in rats

The effect of exercise on the uptake, redistribution, and excretion of iron was studied in normal iron-sufficient rats. Rats were run to exhaustion in a “sprint” protocol seven times over a twentyone day period. Exercised rats did not differ significantly from sedentary rats in hemoglobin concentrations or in body or organ weights. Exercised rats absorbed more iron than sedentary rats in radioiron tracer studies. Radioiron accumulated mainly in heart, liver, and spleen. Strikingly, tracer iron accumulated significantly in hearts of exercised rats. Exercised rats had less total iron in liver and spleen than sedentary rats. Myoglobin concentrations in heart and soleus muscles were significantly higher in rats after the exercise regimen and decreased following fourteen days of rest. Brief, strenuous exercise appears to signal increased absorption of iron and to stimulate the redistribution of storage iron. This mobilization of iron during exercise may be directed towards the enhancement of oxygen-accepting ability in muscles at work.     

The effect of age and dietary restriction on bone strength, calcium and phosphorus contents of male F344 rats

At 6 weeks of age, male Fischer F344 rats were fed a purified, casein based diet either ad libitum or in the amount of 60% of the diet consumed by the rats, fed ad libitum (restricted diet). Femur bone tissues were obtained from the rats at 4 and 13 months of age. The femurs of the animals fed ad libitum were significantly stronger than the femurs of the animals fed a restricted diet both at the age of 4 and 13 months [p0.01]. The body weight and bone weight of the animals fed ad libitum were also higher than that of the animals on the restricted diet. The bone ash weight was significantly lower for food restricted animals [p0.013] when compared to the animals fed ad libitum. The bone phosphorus content was significantly higher in the diet restricted older animals [p0.02] when compared to the diet restricted younger animals. Results indicate that food restriction will delay bone maturation.     

Variations in dietary iron alter brain iron metabolism in developing rats

The rat has been widely used as a model for the study of iron deficiency (ID), but the differences in the timing of development of humans and rats must be taken into account to derive appropriate conclusions from the animal model. This study was designed to evaluate the effects of dietary ID and iron excess on rat brain iron and the iron metabolism proteins, transferrin (Tf), transferrin receptor (TfR) and ferritin. The experimental design is developmentally sensitive and permits control of the timing as well as the duration of the nutritional insult. Iron-deficient and iron-supplemented (SU) rats between postnatal day (PND) 10 and 21, PND 21 and 35 and PND 10 and 35 were used to study the effects of early, late, and long-term iron deficiency and supplementation. Some ID rats were iron repleted between PND 21 and 35. These experiments demonstrated several new findings: 1) Early ID/SU (PND 10-21) altered brain iron, TfR, Tf and ferritin concentration in many regions different from those observed in the later period (PND 21-35). 2) Two weeks of iron repletion were adequate for correcting the overall Fe concentration of the brain and of individual brain regions, although larger amounts of iron were necessary to fully normalize iron and its regulatory proteins. 3) Long-term ID/SU resulted accordingly in the continued decrease or increase in brain iron concentration in some brain regions and not others. In conclusion, brain regions regulate their iron concentration in response to local needs when faced with alterations in systemic iron delivery.     

晕船大鼠体内铁含量的变化

目的　探讨模拟晕船条件下大鼠机体组织铁含量和尿铁排出的变化。方法　将SD大鼠随机分为晕船组和对照组 ,原子吸收分光光度法检测大鼠血清、尿液和部分器官中铁元素的含量。结果　血清、肝脏、大脑、小脑、肾上腺铁含量在对照组依次为 (46 9± 3 5) μmol/L、(94 9± 8 5) μg/g、(3 8 5± 7 5) μg/g、(86 9± 9 5) μg/g、(159 9± 2 1 6) μg/g ,在晕船组依次为 (2 8 1± 4 8) μmol/L、(47 9± 9 1) μg/g、(2 3 6± 6 1) μg/g、(53 0± 8 7) μg/g、(2 96 2± 2 6 5) μg/g ,两组比较 ,差异均具有统计学意义 ;与对照组相比 ,尿液铁在旋转第一天时 ,晕船组大鼠排出量显著减少 ,为 (40 1 4± 2 6 7) μg/d ,第二、三天时显著性增多 ,分别为 (750 7± 2 4 1) μg/d ,(764 3± 2 7 9) μg/d ;而心脏、脑干、下丘脑铁含量与对照组相比有升高的趋势 ,但差异无统计学意义。结论　晕船可能影响大鼠机体铁元素的分布 ,这种变化在晕船发生中的作用值得进一步探索。     

Influences of dietary protein levels and phytate contents on zinc requirement in rats

This study investigates whether the effects of increased dietary levels of soy protein on zinc-deficient rats are due to the dietary protein content. Rats were fed two levels of demineralized soy protein (DP) diets and two levels of egg albumin (EA) diets including 7 ppm zinc (Experiment 1). Growth was depressed in rats fed a 20% DP diet (0.43% phytate) but not in those fed a 10% EA diet containing 7 ppm zinc. Zinc concentrations in the serum, femur and kidney were lower in rats fed the 20% DP diet than those fed a 10% DP (0.20% phytate) diet, and they were also lower in rats fed the 10% EA diet than those fed a 5% EA diet. Zinc concentrations in the serum and femur of rats fed the 10% DP diet or the 20% DP diet were decreased compared with those fed the 5% EA diet or the 10% EA diet, respectively. Under zinc-deficient conditions (<0.4 ppm Zn), the survival time shortened (Experiment 2) and the zinc concentration in the serum and femur decreased faster (Experiment 3) in rats fed the 10% EA diet compared with those fed the 5% EA diet. The survival times and time courses of these parameters show that the zinc requirements of rats increased with the dietary protein level. The increased zinc requirement of rats that accompanied increasing dietary soy protein was due to the dietary protein content as well as the dietary phytate content.