镉致贫血及铁、锌、铜的预防作用

本文探讨了饲镉小鸡发生贫血的性质、原因及补充铁、锌、铜的预防作用。将1日龄雄性京白鸡依体重随机分为6组:对照组、饲镉组、补铁组、补锌组、补铜组及同时补充铁,锌,铜组。实验3周后,测定血红蛋白、红细胞压积、红细胞计数、红细胞脆性、红细胞形态、红细胞游离原卟啉、血浆铜蓝蛋白及肝脏中各元素的浓度。结果表明:1.饲镉小鸡发生了正细胞低色素性贫血,其原因与镉致红细胞变形、渗透脆性增大及机体缺铁、缺铜有关;2.补充铁或铜预防了镉致贫血,补充锌无预防作用;3.饲镉小鸡产生了生长阻滞,补充铁、锌或铜有预防作用。     

甘氨酸亚铁改善大鼠营养性贫血的效果评价

目的　以缺铁大鼠为模型研究了甘氨酸亚铁改善营养性贫血的效果。方法　选择体重5 0 (6 0克二级雌性断乳Wistar大鼠,给予低铁基础饲料耗空3周后,经尾静脉取血,测定血红蛋白含量,按尾血血红蛋白含量,把动物随机分为空白对照组、给予低剂量组、中剂量组、高剂量甘氨酸亚铁组和乳酸亚铁对照组,实验期为4周,测定动物生长发育指标和缺铁性营养性贫血相关指标。结果　补充甘氨酸亚铁显著改善大鼠生长,补充组的终体重和净增重显著高于低铁对照组;甘氨酸亚铁显著升高贫血大鼠的血红蛋白水平,而红细胞内游离原卟啉水平显著降低,补充甘氨酸亚铁组的脾脏铁含量和总铁含量均显著高于低铁对照组,并且与相同剂量的乳酸亚铁相比没有显著差异。结论　甘氨酸亚铁作为一种较理想的补充铁的营养强化剂,可明显改善缺铁性营养性贫血。     

木材加工者体内铜、铁、锌含量的检测结果分析

目的研究木材加工者体内铜、铁、锌含量的变化。方法选择128名从事木材加工业者为接触组,当地65名无木材加工业史的健康居民为对照组,用原子吸收分光光度法测定其血液中铜、铁、锌含量。结果接触组血铜、锌的含量高于对照组(t值分别为18.29和9.46,均P<0.01),并随着工龄的增加呈上升趋势(P<0.01),血铁含量变化不明显(P>0.05),血铜、铁、锌含量与工种间差异无显著性。结论木材加工对作业工人血铜、锌有不同程度影响,铁的变化不明显。     

铁补充对大鼠肝脏铁与叶酸代谢的影响

目的研究缺铁性贫血时机体内叶酸含量的变化及其与铁补充的关系。方法ＳＤ纯品系雄性断乳大鼠３２只，随机分为铁正常、铁缺乏两组。喂纯合成饲料，铁含量分别为８００μｇ与小于２０μｇ，每日两次定时喂饲。两组模型建立后再各取一半大鼠每日补充铁剂８０００μｇ，同前方式每日两次喂饲；另一半大鼠继续原方案不变，共建立铁正常补铁组、铁缺乏补铁组与铁正常、铁缺乏对照４个组；４个实验组每日饲料叶酸含量均小于１０μｇ。结果铁缺乏影响大鼠的一般生长，体重与血红蛋白含量；肝脏重量与肝内铁含量明显低于正常水平，而叶酸含量明显高于铁正常大鼠。补铁后，铁缺乏大鼠的生长、体重、血红蛋白以及肝脏重量明显改善，肝脏的铁含量迅速增加并超出正常水平。在肝脏铁增加的同时，肝脏组织的叶酸含量明显下降，直至显著低于正常。结论提示铁与叶酸同时缺乏的大鼠在补充大剂量铁剂后导致机体内叶酸含量进一步减少，而铁正常大鼠上述变化不明显。     

单纯性维生素A缺乏大鼠模型建立及相关指标观察

目的采用参照AIN-93G纯化饲料要求略加改良配制的维生素A缺乏饲料，建立维生素A缺乏大鼠模型，观察其营养状况及相关指标的变化。方法将雄性SD大鼠（n=16）随机分为正常对照组和维生素A缺乏组。实验至12周，测量血、肝脏维生素A含量及血常规、血生化和血中锌、铁、铜的含量。结果与正常组比较，维生素A缺乏大鼠的总摄食量、血清及肝脏维生素A含量、白细胞总数、血清锌、铜含量明显下降，血清AST、铁含量、锌铜比值显著升高。结论使用该维生素A缺乏动物饲料，可以成功建立维生素A缺乏动物模型，尤其对血中微量元素含量有一定的影响。     

锌及复合微量营养素的营养干预对学龄前儿童蛋白质营养状况的影响

选择重庆市近郊农村学龄前儿童１４０名，男、女各半，随机分为单纯补锌组、补锌及复合微量营养素组和单纯补充微量营养素组，另一组为对照。实验组每组４０人，对照组为２０人，进行１０周营养干预实验。结果显示，在补锌的同时服用硒、锰、维生素Ａ等多种微量营养素或单纯补充多种微量营养素均能有效改善受试儿童体内锌营养状况，使血浆中前白蛋白、转铁蛋白、铜蓝蛋白含量增加，血清中多种必需及非必需氨基酸，３甲基组氨酸浓度下降。提示，儿童营养状况改善后其体内蛋白质合成代谢加强，而分解减少，这种变化除缘于血清锌含量增加外，可能还与其它微量营养素的作用有关。而单纯补锌儿童血清锌变化并不显著，血清中几种转运蛋白与对照均无明显差异。     

赖氨酸、钙、铁、锌强化食品的研究及其营养评价

本实验在面包中强化赖氨酸、钙、铁和锌进行动物实验,评价其营养价值。 实验动物为wistar种系大鼠,4～5周龄,体重相近。随机分为四组、第一组为对照组用普通面包饲养,其余各组分別饲以不同强化面包。 实验结果:对照组四周体重净增59g。单纯加锌组开始两周动物生长加快,以后渐趋抑制,四周后体重净增46g明显低于对照组。加赖氨酸、钙、铁的大鼠生长加快,四周后体重净增91g,饲料效价、蛋白质功效比值、净氮利用率、生物价及骨长和骨重量、铁营养状况均优于对照组。在强化赖氨酸、钙、铁的基础上再补充锌,可进一步促进动物生长,四周后体重净增120g,饲料效价,蛋白质功效比值不但高于对照组也高于赖氨酸、钙、铁强化组,该组饲料中锌对钙、铁生物利用无明显干扰,对血铜亦无显著影响。     

饲喂不同食物的小鼠血清微量元素水平变化的实验研究

目的 :研究饲喂不同食物的小鼠血清中微量元素含量水平的变化。方法 :将小鼠随机分成对照组、实验A组、实验B组 ,分别饲喂正常饲料、加喂鸡蛋、加喂鸡蛋及葵花子仁 ,应用原子吸收光谱法测定 3组小鼠血清中锌、铜、铁、钙、镁的含量。结果 :两个实验组雌、雄小鼠血清中的铁含量水平均对应高于对照组的雌、雄小鼠 ,锌均对应低于对照组 ,锌、铁之间呈负相关。实验B组雌性小鼠的铜、铁均高于实验A组和对照组的雌、雄性小鼠及同组的雄性小鼠。结论 :经常食用鸡蛋、葵花子仁等天然食品 ,可能提高人们特别是妇女体内一些必需微量元素的含量水平 ,有益于人体健康     

男性不育患者血液和精液中微量元素含量分析及相关性研究

目的研究不育男性患者血液和精液中微量元素含量与男性不育的关系。方法将500例不育患者分成实验1、实验2、实验3共3个组别。采用西班牙SCA精子自动检测分析仪、原子吸收光谱仪、7170A全自动生化分析仪,对不育患者和103例正常生育男性的精液进行常规分析,并对其血液和精液中的微量元素进行检测。比较各组间血液和精液中微量元素的含量及各组间血液和精液中微量元素含量的相关性。结果①实验1组血液中镉、铜含量偏高,锌含量偏低,差异有统计学意义;实验2组血液中镉、铜含量偏高,差异有统计学意义;实验3组血液中铜含量偏高,差异有统计学意义。②实验1、2组精液中镉、铜含量偏高,锌含量偏低;实验3组精液中镉、铜含量偏高,差异有统计学意义。③血液和精液中微量元素的相关性:实验1组镉、锌、铜、铁含量呈显著正相关,钙、镁无相关性;实验2组镉、锌、铜含量显著相关,铁、钙、镁无相关性;实验3组镉含量显著相关,锌、铜、铁、钙、镁无相关性。结论血液和精液中微量元素含量过高或过低都会导致男性不育的发生。     

血红素铁胶囊改善大鼠缺铁性贫血状况的研究

目的:研究血红素铁胶囊对大鼠缺铁性贫血的改善情况.方法:以低铁饲料喂饲雌性断乳Wistar大鼠3周建立缺铁性贫血大鼠模型.选血红蛋白含量低于100 g/L的动物随机分4组,10只/组,以20、100、500 mg/kg·BW设置剂量,各组以去离子水稀释,设低铁对照组给予去离子水;各组均喂饲低铁饲料,饮去离子水.比较实验前后血红蛋白、红细胞内游离原卟啉含量及体重的变化.结果:各剂量组均能增加缺铁性贫血大鼠血红蛋白含量;高、中剂量组能明显增加大鼠体重;高剂量组明显降低红细胞内游离原卟啉且与低铁对照组比较均有显著性差异(P<0.05).结论:在研究剂量范围内可见血红素铁胶囊具有改善大鼠缺铁性贫血的功能.     

Cadmium-induced fetal growth retardation in mice and the effects of dietary supplements of zinc, copper, iron and selenium.

Many of the toxic effects of cadmium can be prevented by prior or simultaneous administration of either zinc, copper, iron or selenium. The aim of this investigation was to determine whether cadmium-induced fetal growth retardation in the mouse could be prevented, or reduced, by dietary supplementation with salts of these elements. Pregnant mice, receiving either distilled water to drink or distilled water containing 40 ppm cadmium, were fed, throughout pregnancy, a normal stock mouse diet supplemented with either zinc (200, 400 or 800 ppm), copper (30, 100 or 400 ppm), iron (200 or 1,000 ppm) or selenium (0.05, 2, 20 or 200 ppm). Also included was a control group which did not receive cadmium or dietary supplements. The animals were killed on the 19th day of pregnancy and the fetuses removed and weighed. The results showed that the iron supplemented diets gave partial protection against the cadmium-induced growth retardation; the other diets were ineffective.     

Copper requirement of baby pigs fed purified diets.

Three experiments involving 52 baby pigs were conducted to determine the minimum copper requirement of baby pigs fed purified diets. Diets were supplemented with anhydrous cupric sulfate to yield the following copper concentrations (ppm, by analysis) when the three experiments were combined: 0.6, 0.9, 1.3, 1.9, 2.0, 2.8, 3.2, 4.0, 4.9, 5.6 and 9.3. Parameters examined include weight gain, hematocrit, hemoglobin concentration, mean corpuscular hemoglobin concentration, plasma ceruloplasmin activity, plasma copper concentration, copper balance, brain and erythrocyte superoxide dismutase activity, copper concentration of liver, kidney, spleen, heart, brain, femur and hair, liver ferritin-iron and total iron concentration, strength characteristics of the femur, and gross and histological appearance at necropsy. Weight gains were subnormal at dietary copper concentrations below 1.9 ppm; plasma ceruloplasmin activities, and plasma and tissue copper concentrations were depressed at dietary copper levels below 2.8 ppm. Bone histopathology was evident at dietary copper levels below 3.2 ppm, and copper balance was low at dietary copper levels below 4.9 ppm. Some evidence of anemia was present at dietary copper levels below 5.6 ppm. Under the conditions of this study, the copper requirement of the baby pig fed a purified diet was judged to be approximately 5.6 ppm (6 ppm copper, dry basis).     

Feeding low iron diets affects fluid preference in growing rats

The effect of dietary iron (ferrous sulfate) concentration on the intake of solutions of sodium saccharin, hydrochloric acid, quinine sulfate, sodium chloride, and potassium chloride was studied. Male Charles River CD weanling rats were divided into four groups and fed semi-synthetic iron-free diets supplemented with either 0, 10, 20 or 40 ppm ferrous sulfate. Using a 48 hour, two-bottle preference test, the rats fed the diet with 0 ppm (added) iron showed significantly higher preferences for sodium chloride and potassium chloride solutions compared with the other three groups. Total fluid intake also increased in rats given the unsupplemented diet. Water intake was not increased in this 0 ppm group when sodium was offered. Blood hemoglobin and hematocrit, serum iron and body weight were lowest in the group with 0 ppm added iron, yet neither adrenal weights nor serum zinc was affected by the dietary iron levels.     

膳食中过量锌及锌铁比例对幼鼠的生物学效应

本文对断乳SD雄性大鼠喂饲过量锌及不同锌铁比例的合成饲料30天。结果表明,锌500mg/kg水平时,RBC—SOD活性明显下降,骨锌含量显著增加。锌1000mg/kg水平时,肝铁、骨铁减少,肝脏出现病理改变。过量锌补铁各组肝铁增加,Hb升高,但后者与Zn/Fe无明显关系;虽骨锌下降,但仍高于对照。各实验组肝、骨铜含量无明显变化。     

Long-term effectiveness of dietary iron and ascorbic acid in the prevention and cure of cadmium toxicity in rats.

The protective and curative effects of dietary iron and ascorbic acid on chronic (180 days) cadmium toxicity in rats were examined. Growth retardation and anemia were observed in rats fed a diet containing 50 ppm of cadmium for 180 days; during this period the contents of iron in the liver, kidney, spleen, testis, intestine, and tibia decreased and the zinc contents of the liver and kidney increased, but the calcium content of bone did not change. Addition of 400 ppm of iron and 1% of ascorbic acid to the cadmium-containing diet overcame the growth retardation and anemia due to cadmium toxicity and reduced the tissue levels of cadmium; however, it did not restore the zinc contents in the liver, kidney, and bone to normal. Similar effects were observed when these compounds were added to cadmium containing diet for 90 days after feeding the cadmium diet alone for 90 days. The glutamic-pyruvic transminase and glutamic-oxaloacetic transminase activities in the plasma of rats fed the cadmium diet increased significantly and these increases were prevented by supplementing the diet with iron and ascorbic acid. Glucose, urea, and alkaline phosphatase in the plasma and glycogen in the liver were not changed by feeding the cadmium diet for 180 days. These results indicate the long-term effectiveness of supplementing the diet with iron and ascorbic-acid for preventing and curing dietary cadmium toxicity in rats.     

Utilization of zinc from picolinic or citric acid complexes in relation to dietary protein source in rats

Young male Sprague-Dawley rats were divided in 18 groups of eight animals each and were fed ad libitum for 24 d a purified diet with 20% casein, whey protein or serum albumin as protein source. Each diet was supplemented with zinc picolinate, zinc citrate or zinc sulfate to a level of dietary zinc equal to 5 or 10 ppm. The source of zinc had no significant effect on zinc utilization with any of the three dietary proteins or at either dietary zinc concentration. With the 5 ppm Zn diet zinc concentration in the serum, but not weight gain or the zinc concentration in femur, testis or whole body was lower in rats fed the casein diet than in those fed the whey diet. Zinc concentrations in serum, femur, testis and whole body, but not weight gain, were lower in rats fed the casein diet than in those fed the serum albumin diet. With the 10 ppm Zn diet, zinc concentrations in serum, femur and whole body, but not weight gain nor zinc concentration in testis, were lower in rats fed the casein diet than in those fed either of the other diets. These results suggest that the reason for the lower utilization of zinc from cow milk in comparison to human milk may be the higher casein concentration in cow milk.     

Relationships of dietary zinc/copper ratios to plasma cholesterol and liver trace mineral deposition in young rats fed saturated and unsaturated fats

The effects of copper and zinc supplements on weight gains, plasma total and high density lipoprotein (HDL)-cholesterol levels and liver trace mineral levels were studied in young rats fed either coconut oil or corn oil. Dietary factors included 1.5 ppm and 6 ppm copper, 7.5 ppm and 30 ppm zinc, and the two fat sources. Weight gains and levels of total and HDL-cholesterol were higher in rats fed corn oil than in rats fed coconut oil. Increases in dietary zinc were associated with increases in total and HDL-cholesterol levels in rats fed corn oil, while increases in copper supplements were associated with decreases in total and HDL-cholesterol levels in rats fed either fat source. Supplements of 30 ppm zinc resulted in decreases in total cholesterol/HDL-cholesterol ratios in rats fed coconut oil but had no apparent effect on these ratios in rats fed corn oil. Thus, zinc may be a more important factor than copper in the reduction of this ratio, particularly if saturated fatty acids predominate in the diet. Increases in dietary copper were associated with increases in liver copper levels of rats fed either fat source. Increases in either dietary copper or zinc resulted in decreases in liver iron deposition in rats fed both fat sources. Results of this study indicate that a dietary zinc/copper ratio of 5 may be required for optimum growth of young rats.     

Modification of a selenium toxicity in chicks by dietary silver and copper.

Studies were conducted to determine the effects of high levels of dietary silver nitrate and copper sulfate on the response of chicks to toxic levels of dietary selenium. Adding 5 ppm or more selenium to a basal stock diet significantly reduced growth rate, and 40 ppm or high significantly increased mortality during the 2-week experiments. Deitary silver or copper (1,000 ppm) counteracted the growth depression and prevented mortality at the higher levels of selenium. Hepatic selenium reached a maxiumum in chicks fed the basal diet with 10 ppm dietary selenium. Hepatic selenium of chicks fed silver was less than that of the control chicks when diets containing 10 ppm or less selenium were fed. Adding copper to the diet resulted in considerable accumulation of selenium in the liver, which was evident even at the lower levels of added selenium. Rseults of an experiment to determine the effects of deitray silver and copper on the distribution of 75-Se administered either orally or in tramusculary showed that silver interfered with absorption of selenium. The results of these experiments suggest that silver modifies selenium toxity both by interfering with selenium absorption and by causing the accumulation of a nondeleterious selenium compound in the tissues. Copper modifies selenium toxicity primarily by causing the accumulation of a nondeleterious compound in the tissues.     

Effect of excess L-lysine on rat growth and on plasma and tissue concentrations of copper, iron and zinc

A 28-day feeding study was conducted to test the effect of excess dietary lysine on rat growth and the concentration of copper, iron and zinc in plasma and liver. Young male Sprague-Dawley rats were fed a 10% protein casein diet with or without excess lysine. There were no significant differences in body weight gain, food intake or plasma proteins among the dietary treatment groups. Supplementation of the basal diet with 2.1% L-lysine caused a 53% reduction in hepatic copper and a significant reduction in hepatic iron. The addition of 0.7% or 2.1% lysine to the basal diet caused significant reductions in levels of plasma copper. The 2.1% level of lysine tended to lower the concentration of zinc in plasma. The data suggest that lysine may interfere with the availability of selected minerals by reducing tissue utilization or promoting excretion, or both.     

The effects of sugar-beet fibre supplementation for five weeks on zinc, iron and copper status in human subjects.

The present study was conducted to evaluate the effects of fibre supplementation on zinc, iron and copper status in human subjects. Ten males (53 +/- 8 years of age) participated in this study which consisted of three phases: baseline-1 period (2 weeks) in which subjects were on their normal, habitual dietary intake, followed by a period of fibre supplementation (5 weeks) in which subjects were supplemented with 26 g dietary fibre/d, and baseline-2 period (4 weeks) in which fibre supplement was withdrawn. Parametric measurements of zinc, iron and copper status were conducted on weeks 1,2 (zero-time), 7 and 11. Results showed that fibre supplementation for 5 weeks did not cause any significant change in the status of zinc (measured by concentration of zinc in plasma and urine and alkaline phosphatase activity), iron (measured by packed cell volume (PCV%), HB, transferrin saturation % and ferritin), or copper (measured by plasma copper concentration and erythrocyte superoxide dismutase activity). We conclude that consumption of sugar-beet fibre added to the daily diet does not constitute any risk with respect to zinc, iron and copper nutriture.