铁、铜对过量锌饲养小鸡生物效应的影响

本文对饲料中过量锌对小鸡铁,铜利用的影响以及补充适量铜或铁、铜的预防效果进行了研究。一日龄雄性小鸡喂基础饲料5天后按体重分成4组,用铁锌铜含量不同的实验饲料喂养28天,观察小鸡生长情况及血液生化指标。结果表明,高锌组小鸡生长不良,Hb下降13％,RBC,Hct,MCV均降低、FEP增加,呈现典型小细胞低色素贫血态,血液及肝肾中锌含量增加,铁和铜含量减少;红细胞超氧化物岐化酶和血浆铜兰蛋白活性下降。在含锌饲料中补充铜能改善小鸡的生长状况,体内铜水平及铜依赖酶活性,对改善贫血及体内铁水平的作用不明显。同时补铁则小鸡各项实验指标均得到明显改善。     

6月龄～6岁儿童贫血与全血中铁、钙、铜、铅、镁、锌水平的相关分析

目的分析6月龄~6岁儿童贫血与全血中铁、钙、铜、铅、镁、锌水平相关性,为预防儿童营养性贫血提供依据。方法选取2015年3月—2017年3月到丽水市中心医院门诊体检的6月龄~6岁城区儿童1 804人,采集静脉血进行血常规和铁、钙、铜、铅、镁、锌含量检测,分析贫血与这6种元素含量的相关性。结果丽水城区6月龄~6岁儿童贫血患病率为7.32%,贫血类型以轻度贫血为主,占全部贫血例数的69.70%;6月龄~3岁儿童贫血患病率最高(10.50%)。贫血组儿童缺铁率为41.67%,缺钙率为24.24%,缺铜率为3.03%,均高于非贫血组儿童(P0.05)。全血铁的水平与血红蛋白、红细胞平均体积、红细胞平均血红蛋白量和红细胞平均血红蛋白浓度呈正相关,而与红细胞分布宽度呈负相关(均P0.05)。低铁组儿童钙、铜和锌缺乏率分别为34.43%,1.64%和35.25%,均高于高铁组(P0.05)。结论丽水城区儿童贫血主要发生在6月龄~3岁年龄段,以轻度贫血为主,缺铁是造成儿童贫血的主要原因。     

微量元素三项与红细胞四项在缺铁性贫血诊疗中的应用

目的:探讨微量元素三项及红细胞四项参数在缺铁性贫血中的诊断价值。方法:选择2018年3～2019年3月住院的106名缺铁性贫血患者作为研究组,同时选取常规体检的健康儿童80名作为对照组,检测微量元素铜、锌、铁及红细胞参数血红蛋白、平均红细胞体积、红细胞平均血红蛋白含量、红细胞平均血红蛋白浓度七项检验项目。结果:缺铁性贫血患儿组微量元素铜、锌、铁含量及红细胞参数血红蛋白、平均红细胞体积、红细胞平均血红蛋白含量、红细胞平均血红蛋白浓度均低于健康组,差异具有统计学意义(P0.05)。结论:微量元素铜、锌、铁及红细胞参数血红蛋白、平均红细胞体积、红细胞平均血红蛋白含量、红细胞平均血红蛋白浓度联合检测对缺铁性贫血的诊断具有临床意义,值得推广和应用。     

铁和复合微量营养素改善缺铁性贫血的实验研究

目的 :探讨铁和多种微量营养素改善缺铁性贫血的效果。方法 :用小鼠建立缺铁性贫血动物模型 ,设铁、多种微量营养素 3个补充剂量组和对照组。结果 :铁和复合微量营养素显著提高小鼠的血红蛋白、红细胞压积和血清铁水平 ,并显著降低高剂量组小鼠红细胞内游离原卟啉水平。结论 :在补铁的同时加用铜、锌等多种微量营养素能明显改善缺铁性贫血的症状     

邯郸市某幼儿园540例儿童血液微量元素的含量调查

目的:了解邯郸市某幼儿园儿童微量元素营养状况。方法:对该幼儿园540例1.5～6岁健康儿童进行血液微量元素钙、铁、锌、镉、铅、镁、锰、铜的检测。结果:该幼儿园儿童缺铁性贫血的发生率高达42.41%;钙、锌、镁、锰、铜、铅的异常率较低。发现1例镉超标儿童。各种微量元素的异常在不同性别之间无差异,不同年龄组儿童的铁缺乏情况无统计学差异。结论:该幼儿园儿童的微量元素营养状况基本较好,但要注意铁的补充。     

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。     

实验性镉中毒致小鼠血液学指标改变及硫酸锌的保护作用

目的 探讨亚慢性镉中毒对小鼠血液系统的影响及加锌对镉中毒的拮抗作用.方法选体重16～18 g的小鼠60只随机分成6组,镉染毒的低、中、高和最高4个剂量组分别皮下注射氯化镉溶液(按镉计0.4、0.8、1.6、3.2 mg/kg),每天1次,每周连续4 d,共7周;锌保护组在注射1.6 mg/kg氯化镉的同时饮用ZnSO4(350 μg/L)溶液;阴性对照组注射等量的蒸馏水;染毒结束后测定小鼠的主要血液学指标.结果随着镉染毒剂量的增加,红细胞、血红蛋白、血细胞比容(HCT)、平均红细胞体积、平均红细胞血红蛋白含量等红细胞指标亦逐步下降,其中高、最高剂量组均显著低于对照组和低剂量组(P<0.01或P<0.05);锌保护组以上指标与对照组比较中除HCT指标差异有显著性(P<0.05)外,其余各项指标均接近对照组; 各组白细胞总数随剂量加大逐步升高,最高剂量组升高明显(P<0.01),各组粒细胞比例、单核细胞比例逐步下降,淋巴细胞比例升高;但对血小板影响不明显.结论亚慢性镉中毒能致小鼠贫血(小细胞低色素性贫血),锌能改善镉所致贫血的作用.     

矮小身材儿童全血锌、铜、铁、钙、镁含量分析

目的:观察矮小身材儿童全血锌、铜、铁、钙、镁含量的变化并进行分析。方法:采用火焰原子吸收法检测88例矮小儿童的全血锌、铜、铁、钙、镁含量。结果:矮小儿童的低血锌、低血铜、低血铁、低血钙发生率分别为55.68%、28.41%、51.14%和71.59%,血镁均在正常范围内,未见5种金属元素升高者。低血锌、低血铜、低血铁发生率分别在家族性矮小、GHD、体质性等原因引起的矮小儿中最高,而低血钙率在3组矮小儿间无明显差别。结论:矮小身材儿童体内存在不同程度的锌、铜、铁、钙缺乏,且低血锌、低血铜、低血铁发生率在不同病因中存在差异,故对矮小儿童要注意适当补充锌、铜、铁、钙等金属元素。     

牙龈炎牙周炎患者头发锌铜铁含量比较

目的 :为了解微量元素在牙周病的发生、发展中所起的作用。方法 :用原子吸收法测定患者头发中锌、铜、铁的含量。结果 :牙龈炎组锌、铜、铁的含量均在正常范围内 ,而牙周炎组锌、铁低于正常值 ,铜在正常值以内。讨论 :牙龈炎、牙周炎两组的锌、铁含量有显著差异 ( P<0 .0 5) ,提示 ,铁、锌含量低下 ,是牙周炎发生、发展的重要原因之一     

饲料中的镉对小鸡贫血、铁吸收和镉结合蛋白的影响

动物生长受抑制、贫血、高血压、骨骼矿化减退和肾功能障碍已被证实为镉的毒性作用。其中贫血是最敏感的指标之一。形成贫血的原因,目前尚未完全弄清。在动物饲料中补给亚铁后可防止镉引起的贫血症,因此认为与肠铁吸收有关。本文作者着重研究了饲料中的镉对小鸡铁的吸收、组织中铁的沉积和镉结合蛋白(GdBP)形成所产生的影响。     

Influence of copper and iron on subacute cadmium intoxication in protein-malnourished rats

Male albino rats maintained on low-protein (9%) diets were dosed intraperitoneally with 0.75 mg Cd/kg, as cadmium chloride, for 20 days. Groups of these animals were provided with diets supplemented with 40 ppm Cu, 400 ppm Fe or a combination of both during the exposure period. Hepatic and renal distribution of Cd, Zn, Cu, and Fe along with activity of acid and alkaline phosphatases and ribonuclease and glutathione content were studied. Uptake of Cd both in liver and in kidney was significant and was accompanied by increased Zn and depletion of Fe concentration. The Cu level remained unaltered. Dietary supplementation of Cu or Fe interacted effectively and influenced the metal distribution. Acid and alkaline phosphatases in both liver and kidney were inhibited by Cd exposure. However, Cu and/or Fe supplements could to a varying degree offset the Cd-induced inhibition. Cadmium exposure did not, however, elicit any effect on hepatic and renal ribonuclease activity of low-protein-fed animals. The glutathione concentration registered profound increase on Cd exposure, possibly to act as a defence mechanism.     

Differential Susceptibility to Cadmium-Induced Liver and Kidney Injury in Wild and Laboratory-Bred Bank Voles Myodes glareolus

The objective of the study was to compare the sensitivity of wild and laboratory-bred bank voles to cadmium (Cd)-induced histopathological changes in the liver and kidneys. For 4 weeks, the male bank voles—both wild and laboratory-bred—were provided with diet containing Cd in quantities <0.1 (control), 30, and 60 μg/g dry weight. At the end of exposure period, histopathology and analyses of Cd, metallothionein (MT), glutathione (GSH), zinc (Zn), copper (Cu), iron (Fe), and lipid peroxidation—all considered to be critical factors during the development of Cd toxicity in the liver and kidneys—were carried out. Histopathological changes (focal hepatocyte swelling, vacuolation and inflammation [leukocyte infiltration] in the liver, and focal proximal tubule degeneration [including epithelial cell swelling] in the kidneys) occurred only in the wild bank voles fed a diet containing 60 μg Cd/g. There were no differences in concentrations of Cd, MT, GSH, Zn, and Cu in liver and kidney between the respective groups of wild and laboratory-bred animals. However, a decrease of hepatic Fe and lipid peroxidation was observed in the wild voles exhibiting histopathological changes. These data indicate the following: (1) wild bank voles are more susceptible to Cd-induced liver and kidney injury than those bred and raised in the laboratory; (2) the difference in sensitivity may be associated with a distinct decrease of hepatic Fe in response to Cd exposure between the two groups of bank voles; and (3) dietary Cd may produce histopathological changes indirectly through decreasing the hepatic Fe and Fe-dependent oxidative processes. These results also suggest that histopathology in the liver and kidney of wild bank voles living in a contaminated environment may occur at relatively low levels of tissue Cd.     

The effects of zinc deficiency on turnover of cadmium-metallothionein in rat liver

The object of this experiment was to determine the effects of Zn deficiency on the turnover of Cd-induced metallothionein (MT) in rat liver. Male rats were fed a purified Zn-deficient or Zn-adequate diet. After 13 days, the rats were given three daily injections of Cd2+ totaling 1.5 or 3.0 (Zn-deficient) and 3.0 or 6.0 (Zn-adequate) mg Cd/kg body weight. The MT was labeled by injecting the rats with [35S]cystine 2 hours after the final Cd injection. One, 3 or 5 days after labeling, the rats were killed, and their livers were assayed for MT 35S and metal content. The metal composition of MT (mole %) was 41-42% Cd, 51-54% Zn and 4-7% Cu in the Zn-adequate groups and 64% Cd, 27-31% Zn and 6-9% Cu in the Zn-deficient groups. The half-lives of Cd-induced MT in the Zn-deficient rats were 2.6 days (1.5 mg Cd/kg) and 2.8 days (3.0 mg Cd/kg). In the Zn-adequate rats, the half-lives were 3.6 days (3.0 mg Cd/kg) and 3.1 days (6.0 mg Cd/kg). The half-lives of general, soluble hepatic proteins were 4.1 to 4.3 days in all groups. Despite the stabilizing effect of the higher Cd content, the half-life of hepatic MT in the Zn-deficient rats was significantly shorter than in the Zn-adequate rats. These results indicate that hepatic MT degradation is faster in Zn-deficient animals.     

Dietary copper primarily affects antioxidant capacity and dietary iron mainly affects iron status in a surface response study of female rats fed varying concentrations of iron, zinc and copper.

This study was designed to examine the interactions among dietary iron (Fe), copper (Cu), and zinc (Zn) and their effects on Fe status and oxidative stress in female rats. In a three-factor central composite response surface design, rats were assigned to 15 groups and fed modified AIN-93G basal diets with varying amounts of Fe and Zn (7.0, 15.5, 45.8, 135.6, or 300 micrograms/g diet) and Cu (0.5, 1.1, 3.2, 9.2, or 20 micrograms/g diet) for 6 wk. Variations in hemoglobin, hematocrit, and serum ferritin were mainly related to dietary Fe. Liver nonheme Fe was directly affected by dietary Fe and was slightly attenuated by interactions between Cu and Zn, and Zn and Fe. Serum ceruloplasmin activity was primarily determined by an interaction between Cu and Zn with substantial moderation by the quadratic effect of dietary Cu. Liver and heart total superoxide dismutase (SOD) and Cu/Zn SOD activities were directly affected by dietary Cu. Dietary Fe was the only significant, yet weak, predictor of liver thiobarbituric acid reactive substances (TBARS) and vitamin E content and serum triacylglycerols. Variability in serum Cu was mostly determined by the interaction between Cu and Fe, with modification from the quadratic effect of dietary Cu. Serum Zn varied with dietary Zn with a small negative influence from the interaction between Cu and Fe. In summary, Fe status was minimally influenced by dietary Zn or Cu, and Fe intakes 10-fold greater than required did not induce overt oxidative stress in female rats. In addition, measures of antioxidant capacity were primarily influenced by dietary Cu and were optimal at moderate intakes of this micronutrient.     

Nutraceuticals: A New Challenge against Cadmium-Induced Testicular Injury

Cadmium (Cd) is a widespread heavy metal and a ubiquitous environmental toxicant. For the general population, the principal causes of Cd exposure are cigarette smoking, air pollution and contaminated water and food consumption, whereas occupational exposure usually involves humans working in mines or manufacturing batteries and pigments that utilize Cd. The aim of the present review is to evaluate recent data regarding the mechanisms of Cd-induced testicular structural and functional damages and the state of the art of the therapeutic approaches. Additionally, as the current literature demonstrates convincing associations between diet, food components and men’s sexual health, a coherent nutraceutical supplementation may be a new valid therapeutic strategy for both the prevention and alleviation of Cd-induced testicular injury. The toxic effects on testes induced by Cd include many specific mechanisms, such as oxidative stress, inflammation and apoptosis. As no specific therapy for the prevention or treatment of the morbidity and mortality associated with Cd exposure is available, the development of new therapeutic agents is requested. Dietary strategies and the use of nutraceuticals, particularly abundant in fresh fruits, beans, vegetables and grains, typical of the Mediterranean diet, are recommended against Cd-induced testicular injury.     

Binding of endogenous copper and zinc to cadmium-induced metal-binding proteins in various tissues of Perna viridis

Green lipped mussels, Perna viridis, were exposed to cadmium chloride (CdCl2; 0.52 and 1 g/ml) in water for 4 days. The concentrations of cadmium (Cd), copper (Cu) and zinc (Zn) were measured in the viscera, gill, gonads, mantle, and muscle. There was a significant increase (p<0.05) in Cd concentration in all tissues studied. Results from Sephadex G-75 chromatography indicated that most Cd was bound to a fraction of heat-stable proteins similar to the metal-binding protein (MBP) metallothionein. After exposure to Cd, there was no significant change in Cu concentration in total tissue proteins or in total cytosolic proteins. A significant increase (p<0.05) in Cu, however, was detected in heat-stable proteins bound to the Cd-induced MBP in both viscera and gill. Copper bound to MBP also occurred in the gonad, mantle, and muscle, but to a much lesser extent. These results showed that Cd-induced MBP can also bind endogenous Cu. Zinc concentration in total heat-stable protein was increased only in gill and the muscle. Unlike Cu, a small amount of Zn binding to Cd-induced MBP was detected only in these tissues. Considering that both Cu and Zn exist intracellularly in dynamic equilibrium, the binding of Cu, but not Zn, to MBP may be explained by the kinetic reactivity of the two different metals to protein. The results of this study support the thesis that induction of intracellular MBP may also bind endogenous Cu and Zn.     

Effect of zinc deficiency on the accumulation of metallothionein and cadmium in the rat liver and kidney

The effects of zinc (Zn) deficiency and repeated exposure to cadmium (Cd) on the accumulation and distribution of metallothionein (MT), Cd and Zn in the liver and kidney were studied. Male Sprague-Dawley rats were fed either a Zn-deficient (1 ppm) or a Zn-adequate (40 ppm) diet during the experiment, and the rats were injected subcutaneously with a cadmium chloride solution (1.0 mg Cd/kg of body weight, 5 days a week) for 4 weeks. Cadmium, Zn, and Cd-induced MT concentrations in the liver and kidney were lower in the Zn-deficient rats (–Zn + Cd) than in the Zn-adequate rats (+ Zn + Cd), while the content of Cd bound to high molecular weight proteins (HMWP) was greater in the Zn-deficient rats (–Zn + Cd). The Zn bound to Cd-induced MT was reduced to 30% in the liver and to 60% in the kidney of the Zn-deficient rats (–Zn + Cd) as compared with that of the Zn-adequate rats (+ Zn + Cd). In the kidney of Zn-deficient rats, exposure to Cd caused a decrease in essential Zn associated with HMWP as compared with that of Zn-adequate rats (+ Zn + Cd). Thus, Zn-deficiency affected the distribution of Cd in tissues, MT and HMWP and accelerated substantially Cd-induced Zn-deficiency in the kidney. Although the renal Cd concentration was lower in the Zn-deficient rats (–Zn + Cd) than in the Zn-adequate rats (+ Zn + Cd), exposure to Cd for four weeks resulted in glucosuria and an increase in liver and kidney weights in the Zn-deficient rats (–Zn + Cd), but not in the Zn-adequate rats (+ Zn + Cd). These results suggest that development of Cd toxicity is related to the Zn status of the body, to the accumulation of Cd in HMWP and to the amount of essential Zn associated with HMWP.     

Anemia induced by cadmium intoxication

Anemia is commonly induced by chronic cadmium (Cd) intoxication. Three main factors are involved in the development of Cd-induced anemia: hemolytic, iron-deficiency, and renal. Intravascular hemolysis can occur at the early stage of Cd exposure owing to the direct damaging effect on erythrocytes. In addition, Cd that accumulates in erythrocytes affects membrane cytoskeletons and decreases cell deformability, and these cells are then trapped and destroyed in the spleen. Iron deficiency can be detected in animals after an oral exposure to Cd, which competes with iron for absorption in the intestines, leading to anemia. However, an increase in body iron content along with anemia is often observed in cases of parenteral exposure or itai-itai disease. Therefore, it is estimated that Cd disrupts the efficient usage of iron in hemoglobin synthesis in the body. Renal anemia is observed during the very last phase of chronic, severe Cd intoxication, such as itai-itai disease, showing a decrease in the production of erythropoietin from renal tubular cells. Because the renal anemia is based on the same pathophysiology as Cd-induced osteomalacia, which is derived from the disturbance of mineral metabolism due to renal tubular dysfunction, it is reasonable to include renal anemia in the criteria for the diagnosis of itai-itai disease. Hemodilution could also contribute to the development of Cd-induced anemia. Bone marrow hypoplasia or the inhibition of heme synthesis might only be involved in Cd-induced anemia in severe cases of Cd intoxication.     

Zinc-induced anemia in young japanese quail ameliorated by supplemental copper and iron

Studies were conducted to examine whether anemia induced in newly hatched Japanese quail by moderate dietary Zn supplements could be corrected by supplemental Fe, Cu, or Mg by 14 d of age. Low hemoglobin (Hb) was partially alleviated by increased levels of Fe or Cu, but normal Hb was obtained only with Fe plus Cu. Fe and Cu concentrations in the liver were decreased at 7 d, prior to the development of anemia by 13 d. Additional Mg had no effect on low Hb caused by Zn. Copper supplementation partially alleviated the growth depression and entirely prevented the lack of feather pigmentation that resulted from Zn toxicosis. Neither Fe nor Mg affected either of these parameters. These data indicate that both Fe and Cu status of an individual may be compromised by dietary Zn supplementation.     

The effect of low doses of dietary cadmium oxide on the disposition of trace elements (zinc,copper, iron), hematological parameters,and liver function in rats

The Zn, Cu, and Fe concentrations in selected organs, tissues and in the excreta of male Wistar rats, exposed to dietary CdO (2.80 and 7.15 ppm) for 40 and 60 days, were investigated. Concomitantly hematological values and serum enzyme activities were recorded. Zn levels of spleen, kidney, testes, muscle and feces were not affected by the Cd treatment. After 40 days of Cd exposure, the Zn concentration in the hair decreased, while the Zn level of the lung slightly increased. During the feeding trial, Cd produced an increase of liver Zn by about 24%. Femur Zn decreased and Zn in urine increased after 60 days of exposure to 7.15 ppm Cd. Except in hair and urine, the Cu concentration in all organs and tissues investigated remained unchanged. Hair Cu levels decreased after 40 days of Cd exposure but increased after 60 days. At this time, elevated Cu concentration in urine was recorded. After exposure to 7.15 ppm Cd, the Fe content of the lung, liver, spleen, testes, muscle, femur and blood decreased significantly. After 60 days on the 7.15 ppm diet, highest reductions (30%–60%) of Fe content were recorded in the lung, liver, and spleen. Similar to Zn and Cu, the Fe concentration in urine increased at that time. No changes were found in the Fe content of hair, kidney, and feces. In spite of a disturbed Fe metabolism, an anaemic response of Cd-treated rats was not observed. Hematocrit and hemoglobin remained unchanged and the number of red blood cells slightly increased after 40 days of Cd exposure. While the activity of serum alkaline phosphatase was not affected by dietary Cd, the activities of serum-GOT and serum-GPT increased after exposure to 7.15 ppm Cd indicating disturbed hepatic functions.