Cadmium Interaction with Essential Metals (Zn, Cu, Fe), Metabolism Metallothionein, and Ceruloplasmin in Pregnant Rats and Fetuses

Cadmium administered to rats per os is accumulated in the duodenal mucosa in the form of metallothionein (MT). Therefore, this toxic metal can influence the efficiency of essential metal absorption, especially their concentration in the maternal organism, which plays an essential role during fetal development. The aim of this study is to elucidate the mechanism of the origin of Zn, Cu, and Fe deficiency in fetal rat livers after maternal exposure to cadmium in drinking water and to investigate the roles of MT and ceruloplasmin (Cp) in this phenomenon. Cadmium was given to pregnant dams exposed for 0–20 days of gestation in drinking water at concentrations of 6.25–100 μg Cd/ml. After cessation of exposure, at the lowest dose, a decrease in Cu and Fe concentrations in the duodenal mucosa was found. Simultaneously, diminution in concentration of two cited metals and Cp activity in serum of dam blood was noted. The lowest dose of cadmium developed a drop tendency in microsomal fetal liver iron. Significant correlations were observed between fetal liver Cu contents and Cp activity in serum of dams and Cu concentrations in serum of dams. Diminished Cp activity in serum of dams is related to reduced availability of Cu and Fe in fetuses. In conclusion, it is suggested that the mechanism of Cu and Fe deficit content in fetuses is based on the diminution of absorption of these metals by dam intestines exposed to cadmium on the reduction of metal concentrations in blood serum and, in consequence, their decreasing availability in fetuses.     

Hepatic glutathione, metallothionein and zinc in the rat on gestational day 19 during chronic ethanol administration

Ethanol, under certain conditions, alters the metabolism of sulfur amino acids, metallothionein (MT) and zinc. If chronic ethanol administration during pregnancy decreases the availability of sulfur amino acids or Zn, this deficiency could contribute to growth retardation of the fetuses, one of the features of fetal alcohol syndrome. The purpose of this study was to discern whether chronic ethanol administration to pregnant rats alters glutathione (GSH), MT or Zn content of selected tissues of the dams and fetuses. Sprague-Dawley rats were fed from gestational days 5 to 19 either the control diet ad libitum (AF), the ethanol diet ad libitum (EF) or the control diet using the pair-feeding technique (PF). On the 19th day of gestation, total hepatic GSH was significantly lower for the EF and PF dams than for the AF dams. Hepatic MT contents were similar for the AF and EF dams, and hepatic MT content was significantly greater for the PF dams than the AF and EF dams. The three groups did not differ regarding hepatic Zn content of dams or fetuses. In summary, on the 19th day of gestation, chronic ethanol feeding of pregnant rats did not lower the maternal hepatic GSH level below that of PF dams, did not induce hepatic MT in the dams and did not prevent fetuses from achieving body weights and hepatic Zn concentrations equal to those of controls.     

Comparative study of effect of acute administration of cadmium and silver on ceruloplasmin and metallothionein: Involvement of disposition of copper,iron, and zinc

Male ICR mice were subcutaneously injected with either aqueous Ag (1.5 or 5.0 mg/kg) or Cd (1.5 or 2.5 mg/kg) for 2 consecutive days. Body fluids and livers were collected 24 hr after the second dose. In the hepatic supernatant, Ag and Cd were recovered at 2 and 36–46% of the total dose, respectively. Ag-metallothionein (MT), which is associated with Ag, Cu, and Zn, and Cd-MT, which is associated with Cd, Cu, and Zn, were induced in the liver by the injection of Ag and Cd, respectively. The supernatant Ag and Cd existed in the MT fraction at 34–61 and 97% levels, respectively. Cu concentration in the hepatic supernatant was increased by the Ag and Cd injections. The increased Cu was due to the appearance of Ag-MT and Cd-MT, respectively. Microsomal concentrations of Cu increased in the Cd groups, but decreased in the Ag groups. Serum ceruloplasmin (Cp) activity was remarkably increased by the injection of Cd, but severely decreased by the injection of Ag. These opposing changes in Cp activity induced by Cd and Ag may be due not to the sequestering of Cu in MT, but to the alteration of microsomal Cu concentration and/or the difference in affinity of the induction metals to MT. Hepatic Fe concentration was increased by the Ag injection, but was decreased by the Cd injection. These changes may not be related to induction of MT, but to Cp synthesis in the liver.     

Marginal maternal Zn intake in rats alters mammary gland Cu transporter levels and milk Cu concentration and affects neonatal Cu metabolism

Marginal zinc intake is common and leaves women particularly vulnerable to Zn deficiency due to increased demand for Zn as a consequence of reproduction. Zn deficiency during pregnancy and lactation has been associated with secondary affects on copper metabolism in the offspring; however, the underlying mechanisms are unknown. The effects of marginal maternal Zn intake on maternal and neonatal Cu metabolism were determined in rats. Plasma, milk and tissue Cu and Zn concentrations and plasma and milk ceruloplasmin (Cp) activity were measured in dams fed a control (CON, 25 mg Zn/kg diet) or a marginal Zn diet (ZD, 10 mg Zn/kg diet) and their suckling pups. There was no effect on maternal tissue Cu or Zn or milk Zn concentration; however, plasma Cp activity was higher in dams fed ZD, suggesting that Cp activity may be a useful marker for identifying marginal Zn status. Rats fed ZD had high mammary gland Ctr1, Atp7A and Atp7B levels, milk Cp activity and Cu concentration. Immunostaining and differential centrifugation indicated that ZD also altered Ctr1 and Atp7A localization in the mammary gland. Pups from dams fed ZD had higher small intestine Cu and lower plasma Cu than CON pups. These results suggest that marginal maternal Zn intake during pregnancy and lactation increase mammary gland Cu transporter levels and alter their localization, resulting in high milk Cu levels, possibly in response to transiently elevated plasma Cu levels. The combination of high milk Cu concentration and immature neonatal Cu transport exposes the suckling neonate to excess Cu; however, whether this occurs in humans is not yet known.     

Iron and zinc concentrations and 59Fe retention in developing fetuses of zinc-deficient rats

Because disturbances in iron metabolism might contribute to the teratogenicity of zinc deficiency, we examined the effect of zinc deficiency on fetal iron accumulation and maternal and fetal retention of 59Fe. Pregnant rats were fed from mating a purified diet containing 0.5, 4.5 or 100 micrograms Zn/g. Laparotomies were performed on d 12, 16, 19 and 21 of gestation. Maternal blood and concepti were analyzed for zinc and iron. Additional groups of dams fed 0.5 or 100 micrograms Zn/g diet were gavaged on d 19 with a diet containing 59Fe. Six hours later maternal blood and tissues, fetuses and placentas were counted for 59Fe. Maternal plasma zinc, but not iron, concentration was affected by zinc deficiency on d 12. Embryo zinc concentration on d 12 increased with increasing maternal dietary zinc, whereas iron concentration was not different among groups. On d 16-21 plasma iron was higher in dams fed 0.5 micrograms Zn/g diet than in those fed 4.5 or 100 micrograms/g, whereas plasma zinc was lower in dams fed 0.5 or 4.5 micrograms Zn/g than in those fed 100 micrograms Zn/g diet. On d 19 zinc concentration in fetuses from dams fed 0.5 micrograms/g zinc was not different from that of those fed 4.5 micrograms/g zinc, and iron concentration was higher in the 0.5 microgram Zn/g diet group. The increase in iron concentration in zinc-deficient fetuses thus occurs too late to be involved in major structural teratogenesis. Although whole blood concentration of 59Fe was not different in zinc-deficient and control dams, zinc-deficient dams had more 59Fe in the plasma fraction.(ABSTRACT TRUNCATED AT 250 WORDS)     

Maternal protein restriction and fetal growth: lack of evidence of a role for homocysteine in fetal programming

The disease-programming effects of a maternal low-protein (MLP) diet in rat pregnancy have been suggested to be attributable of hyperhomocysteinaemia. The aim of the present study was to determine whether MLP feeding impacted upon maternal and day 20 fetal homocysteine concentrations, with ensuing effects upon oxidant/antioxidant status. Sixty-four pregnant rats were fed either MLP diet or control diet before termination of pregnancy at days 4, 10, 18 or 20 gestation (full-term gestation 22 d). Maternal plasma homocysteine concentrations were similar in control and MLP-fed dams at all points in gestation. Fetal plasma homocysteine was similarly unaffected by MLP feeding at day 20 gestation. Activities of superoxide dismutase and glutathione peroxidase were similar in livers of mothers and fetuses in the two groups. Whilst catalase activity was not influenced by diet in maternal liver, MLP exposure increased catalase activity in fetal liver at day 20. Oxidative injury (protein carbonyl concentration) was lower in the livers of MLP-fed animals at day 18 gestation (P<0.05), but significantly greater at day 20. Hepatic expression of methionine synthase was similar in control and MLP-fed dams at all stages of gestation. Expression of DNA methyltransferase 1 in fetal liver was altered by maternal diet in a sex- and gestational age-specific manner. In conclusion, MLP feeding does not impact upon maternal or fetal homocysteine concentrations prior to day 20 gestation in the rat. There was no evidence of increased oxidative injury in fetal tissue that might explain the long-term programming effects of the diet.     

Zinc-induced metallothionein and copper metabolism in intestinal mucosa, liver, and kidney of rats

Large doses of parenteral zinc (Zn) and/or the feeding of high Zn diets to animals or humans for long periods affects copper (Cu) metabolism. Previous work suggests that Zn-induced metallothionein (MT) in intestinal epithelial cells binds Cu and inhibits its absorption. This study was designed to determine the effects of treating rats with high dietary or parenteral Zn on Cu metabolism and its relationship to MT in the intestinal epithelium, liver and kidney. Six-week-old male rats were fed for one week a control diet containing 42 mg Zn and 6 mg Cu/kg. They were then divided into three groups. One group continued to receive the control diet while another received a similar diet containing 560 mg Zn/kg. A third group, fed the control diet, received a subcutaneous dose of 90 mg Zn/kg body weight every 2–3 days for the duration of the experiment. Rats from each group were killed on days 7 and 14. Low Cu status in Zn-treated rats was indicated by lower than normal serum Cu concentration, serum ceruloplasmin activity, low liver and kidney Cu concentrations and low cytochrome C oxidase activity. None of these changes, however, were related to an increase in Cu as a result of Zn-induced MT in the intestinal epithelial cell. Instead, as the MT concentrations rose, Cu concentration decreased. This study suggests that the effects of high Zn treatment on Cu status are not the result of the long-held theory that Zn-induced intestinal MT sequesters Cu and prevents its passage to the circulation. Instead, it may be caused by a direct effect of high lumenal Zn concentrations on Cu transport into the epithelial cell.     

Effect of experimental zinc deficiency and repletion on sodium, potassium, copper and iron concentrations in guinea-pigs

Zinc, sodium, potassium, copper and iron concentrations were analysed in serum and tissues of guinea-pigs fed on a diet containing 1.25 mg Zn/kg diet over a period of 60 d. The response of the Zn-deficient (ZnD) animals to Zn supplementation (100 mg Zn/kg diet) was also studied for 15 d. Serum studies in the ZnD group revealed significant decreases in the concentrations of Zn and Na from 24 d, and increases in the concentrations of Fe and K from 36 and 48 d onwards respectively; an increase in Cu was seen on day 60 only. Zn deficiency caused significant reductions in Na, K and Zn and increases in Cu and Fe contents of liver and kidney. In testis, significant decreases were noted only in Zn, K and Fe contents. Zn supplementation of the previously ZnD group resulted in marked improvements in serum and tissue mineral levels. However, hepatic Cu and Fe and renal K did not appear to respond appreciably.     

Iron-induced metallothionein in chick liver: a rapid, route-dependent effect independent of zinc status

The induction of hepatic metallothionein (MT) by the parenteral administration of iron was studied. Iron administered to chicks by intravenous or subcutaneous injection caused a 1.9-fold increase in hepatic MT. In marked contrast, intraperitoneal (ip) Fe resulted in a 10-fold increase, thus demonstrating the importance of the route of metal administration. This route-dependent effect was found to be dose-dependent, with ip injections between 1 and 10 mg Fe/kg resulting in a linear increase in MT and a concomitant reduction in serum zinc concentration and feed intake. High ip doses of Fe resulted in a persistent depression in serum Zn and elevated MT and MTmRNA. Equimolar ip injections of either Zn or Fe showed similar patterns of MTmRNA accumulation. In both cases MTmRNA levels were elevated by 3 h, with a peak at 6 h postinjection (Fe 8-fold, Zn 12-fold above 0 h). Plasma Zn was maximally reduced by Fe at 9 h (60%). The MT induction by Fe, as well as related depression in plasma Zn, was completely inhibited by actinomycin D. Zn depletion eliminated the accumulation of hepatic Zn and MT protein following ip injection of Fe or endotoxin, but not of cadmium, despite marked elevation of hepatic MTmRNA. Our results demonstrate Fe injected into the body cavity of chicks results in a rapid induction of hepatic MT that, like endotoxin induction, is independent of dietary Zn status.     

Changes in dietary zinc result in specific alterations of metallothionein concentrations in newborn rat liver

To investigate the role of metallothionein (MT) in the sequestration and storage of zinc in newborn rat livers, a cross-fostering experiment was performed in which zinc-deficient (Zn-D) pups were suckled from Zn-sufficient (Zn-S) dams and vice versa. At consecutive days during lactation, groups of pups were killed. The experiment was continued for 22 d. Zinc concentrations in various tissues and MT concentrations in livers and kidneys were analyzed. The retention of injected 65Zn, as well as body weight, was also studied in both groups. Higher whole-body retention of 65Zn in the zinc-depleted (Zn-Dp) rats indicates a decreased zinc turnover. These rats also showed markedly reduced growth. The observation that the zinc-repleted (Zn-Rp) pups, although showing 65Zn retention similar to that of controls, grew less than controls suggests that Zn-Rp may not compensate for gestational zinc deficiency. Zn-Rp pups showed an increased accumulation of zinc into hepatic MT until d 10, whereas Zn-Dp pups showed a more accelerated degradation of MT than controls. These data indicate that hepatic MT levels fluctuate directly in response to dietary zinc status in newborn rats. Various tissues such as spleen, heart, lung and intestine showed no difference in zinc concentration among all groups at d 22 postpartum. Thus the rapid degradation of hepatic MT in zinc deficiency that may occur to maintain the required zinc levels in other tissues supports the role of MT as a zinc storage protein in newborn rats.     

Tissue Distribution of Metals in White-fronted Geese and Spot-Billed Ducks from Korea

This study presents concentrations of Fe, Zn, Mn, Cu, Pb and Cd in livers, kidneys, muscles and bones of white-fronted geese Anser albifrons (geese) and spot-billed ducks Anas poecilorhyncha (ducks). Iron in livers, kidneys and muscles, Zn in muscles, Mn and Cd in every tissue, Cu in livers, muscles and bones and Pb in bones differed between species, and there were significant differences among tissues in both species. Essential elements such as Fe, Zn, Mn and Cu concentrations were within the background levels. Lead concentrations in livers of 7 of 14 geese and 7 of 19 ducks and in bones of 4 of 19 ducks exceeded background concentrations for waterfowl (5 μg/g dw for the liver, 10 μg/g dw for the bone). Almost all samples of both species had the background Cd concentrations in the liver (33 of 33 geese and ducks) and kidney (14 geese and 18 ducks). Tissue concentrations of Cd were greater in geese than ducks. In contrast, tissue concentrations of Pb in bones were greater in ducks than in geese. These different trends for Cd and Pb reflect a short and/or long term difference in exposure and degree of accumulation of these metals.     

Effect of dietary copper deficiency on iron metabolism in the pregnant rat

Cu and Fe metabolism are known to be linked, but the interactions during pregnancy are less well studied. In the present study we used rats to examine the effect of Cu deficiency during pregnancy on Fe and Cu levels in maternal and fetal tissue and on the gene expression profile of proteins involved in Cu and Fe metabolism in the placenta. Rats were fed diets with different Cu contents before and during pregnancy. Samples were collected on day 21 of gestation. Cu levels, ceruloplasmin activity and serum Fe all decreased in maternal serum of Cu-deficient animals. Maternal liver Fe inversely correlated with liver Cu. Placental Cu levels decreased with no change in Fe. Fe and Cu levels both decreased in the fetal liver. The drop in maternal liver Cu was significantly correlated with a decrease in organ weight of fetal liver, lung and kidney. No changes were observed in mRNA expression of Cu transporter 1, Menkes P-type Cu-ATPase 7A, Wilson P-type Cu-ATPase 7B, cytochrome-c oxidase, and Cu chaperone Atox1 in the placenta of Cu-deficient dams. Transferrin receptor 1 and the Fe-responsive element (IRE)-regulated divalent metal transporter 1 (DMT1) were up regulated; while ferroportin and non-IRE1-regulated DMT1 levels did not change. These data show that Cu deficiency during pregnancy not only has a direct effect on Fe levels but also regulates the expression of Fe transporters. The pattern closely mirrors that seen in Fe deficiency, suggesting that the changes are a consequence of the decrease in serum Fe, implying that the developing fetus not only suffers from Cu, but also from Fe deficiency.     

Effects of copper supplementation on ceruloplasmin and copper-zinc superoxide dismutase in free-living rheumatoid arthritis patients.

Inflammation, an acute phase stress, alters copper (Cu) metabolism, but effects on human Cu requirements are unknown. Cu supplementation (2 mg/day, 4 weeks) increased erythrocyte Cu-zinc (Zn) superoxide dismutase (SOD) activity levels in 18 of 23 rheumatoid arthritis (RA) patients receiving gold or methotrexate (mean increase 21%). SOD values were significantly lower in RA patients than in 47 age- and sex-matched controls before, but not after supplementation. Supplementation did not significantly affect ceruloplasmin (Cp) activity or protein concentrations in either group. However, RA subjects showed significantly lower Cp activity to protein ratios compared to controls, before and after supplementation. Cu supplementation did not affect acute phase status of RA patients as evidenced by unchanged serum alpha-1-acid glycoprotein levels. In conclusion, the effects of Cu supplementation on erythrocyte SOD activities suggested a trend toward marginal Cu status in RA patients.     

Ultrasound evaluation of fetuses of zinc-deprived monkeys (Macaca mulatta).

Fetal body movements were studied in three groups of gravid rhesus macaques fed different amounts of dietary zinc (100 micrograms Zn/g diet, control, n = 12; 4 micrograms Zn/g diet, marginal deprivation, n = 7; 2 micrograms Zn/g diet, moderate deprivation, n = 11). Sonographic examinations were conducted during the third trimester in awake chair-restrained dams. Movement categories, derived from the human biophysical profile, were motor activity (trunk and limb movements), startle, and breathing movements. Moderately deprived fetuses were more active than controls on gestational day (GD) 115; maternal plasma zinc concentrations were significantly correlated with fetal activity at this time. In addition moderately deprived fetuses exhibited fewer breathing episodes on GDs 115-135. Biometrics measures indicated growth retardation in one moderately deprived fetus. These data suggest that moderate, but not marginal, dietary zinc deprivation influences fetal status as evaluated by sonography.     

Folate deficiency during pregnancy impacts on methyl metabolism without affecting global DNA methylation in the rat fetus

The methionine cycle and methyl group metabolism are implicated in the long-term programming of metabolism. Diets deficient in folic acid, methionine and choline have been fed to pregnant rats to examine the effects on amino acid metabolism, choline reserves and DNA methylation in dam and fetuses. Animals were fed folate-deficient, folate-deficient with low methionine, folate-deficient with low choline and folate-deficient, low-methionine, low-choline diets starting 2 weeks before mating. The dams and their fetuses were subsequently killed on day 21 of gestation for analysis. Diets low in methionine reduced fetal and maternal weight. Folate deficiency increased the concentrations of homocysteine, glycine, serine and threonine in the maternal plasma, and this was exacerbated by the low-methionine diets. The changes in the amino acid profile in the fetal serum were similar but less pronounced. This result suggests that fetal metabolism was less perturbed. Folate deficiency increased free choline in the maternal liver at the expense of phosphocholine stores. It has been suggested that a deficiency in methyl donors in the diet during pregnancy may impact on key methylation reactions, including the methylation of DNA. Despite widespread changes in the metabolism of choline and amino acids, there was no change in the global methylation of cytosine in DNA from either maternal or fetal livers. This suggests a more indirect mechanism in which gene-nutrient interactions modify the process of differential methylation during development.     

Coaccumulation of Cadmium and Zinc in Tissues of Sentinel Mallards (<Emphasis Type="Italic">Anas platyrhynchos</Emphasis>) Using a Former Dredge-Disposal Impoundment

Six- to eight-month-old female farm-raised mallards (Anas platyrhynchos) were used to examine the accumulation of and association among cadmium (Cd), zinc (Zn), and copper (Cu) from an impoundment constructed to contain sediments dredged from a lake contaminated by a zinc smelter. Cd was not detectable in the livers t of farm-raised mallards (day 0), although sentinel mallards accumulated hepatic Cd in the first 7 days after release. By day 14, mean concentrations of Cd in kidneys (= 2.82 mg/kg wet weight) had increased 3.4-fold. The mean pancreatic Cd concentration increased 59% between days 7 and 14. Renal Zn increased nominally, whereas pancreatic Zn increased 63% in sentinel ducks after release. Hepatic Zn increased significantly in the first week of release. Renal and pancreatic Cu concentrations did not change significantly, whereas concentrations of Cu in livers of ducks increased 50% in the 7 days after release before decreasing by nearly the same degree. Concentrations of Cd and Zn were correlated in livers of sentinel mallards on days 7 and 14. Cd and Cu were not correlated in the tissues of any cohort. Cu and Zn were correlated in the livers of farm-raised mallards, in the pancreases of sentinel mallards at day 7, and in the kidneys of the ducks in all three treatments. The relationship between Cd and Zn in tissues of ducks in our study was complicated by simultaneous exposure to increased and heterogeneous concentrations of Cd and Zn, both of which can induce metallothionein and compete for this and other ligands. L. M. Skowron retired     

Metal-metal interactions of dietary cadmium, copper and zinc in rainbow trout, Oncorhynchus mykiss

The influence of metal-metal interactions on uptake, accumulation, plasma transport and chronic toxicity of dietary Cu, Cd and Zn in rainbow trout (Oncorhynchus mykiss) was explored. Juvenile rainbow trout were fed diets supplemented with (μg/g) 500 Cu, 1000 Zn and 500 Cd singly and as a ternary mixture at 2.5% body weight daily ration for 28 days. Complex interactions among the metals dependent on the tissue/organ, metals ratios and duration of exposure were observed. While Zn did not accumulate, whole-body Cd and Cu concentrations increased following linear and saturation patterns, respectively. Early enhanced whole-body Cu accumulation in fish exposed to the metals mixture was correlated with reduced Cd concentration whereas late enhancement of Cd accumulation corresponded with elevated Cd concentration. This suggests early mutual antagonism and late cooperation between Cd and Cu probably due to interactions at temporally variable metal accumulation sites. At the level of uptake, Cd and Cu were either antagonistic or mutually increased the concentrations of each other depending on the duration of exposure and section of the gut. At the level of transport, enhanced Cd accumulation in plasma was closely correlated with reduced concentrations of both Zn and Cu indicating competitive binding to plasma proteins and/or antagonism at uptake sites. Compared to the Cu alone exposure, Cu concentrations were either lower (gills and carcasses) or higher (liver and kidney) in fish exposed to the metals mixture. On the other hand, Cd accumulation was enhanced in livers and carcasses of fish exposed to the mixture compared to those exposed to Cd alone, while Zn stimulated Cu accumulation in gills. Chronic toxicity was demonstrated by elevated malondialdehyde levels in livers and reduced concentrations of Zn and Cu in plasma. Overall, interactions of Cd, Cu and Zn are not always consistent with the isomorphous competitive binding theory.     

Hepatic Metal and Metallothionein Levels in a Potential Sentinel Teleost,Dulesauriga, from a Southeastern Brazilian Estuary

The identification of estuarine sentinel species is of paramount importance. The potential of the species Dules auriga sampled from Guanabara Bay, Brazil regarding metal contamination was assessed. Hepatic metallothionein (MT) and Fe, Zn, Cu, Mn, Cd and Ag concentrations were determined in cytosolic fractions (S50 and HT S50) by polarography and ICP-OES, respectively. HT S50 Fe, Mn and Zn were lower than in the S50 fraction, indicating MT-detoxification. MT was correlated to HT S50 Zn, indicating Zn homeostasis. Zn was negatively correlated to weight (TW) and length (TL), suggesting environmental Zn influence. A moderate negative correlation between HT S50 Cu and the condition factor (CF) was observed, indicating that increasing environmental Cu concentrations may decrease D. auriga CF. Several inter-elemental correlations were observed. No MT, TW and TL correlations were found. Thus, MT variability is probably linked to environmental metal concentrations. D. auriga fulfills most sentinel requisites, and MT may be an adequate metal contamination biomarker in this species.

     

晚期孕妇铁、锌、铜营养状况与贫血的关系

目的：了解晚期孕妇血清铁、锌、铜营养状况和缺铁性贫血的关系。方法：对在1999年12月-2000年2月期间来福建省福清市医院和妇幼保健院门诊检查的242名晚期孕妇采取空腹静脉血10ml，测定血红蛋白（Hb）、红细胞压积（Hct）和血清铁（Fe）、锌（Zn）、铜（Cu）、铁蛋白（SF）、可溶性转铁蛋白受体（s-TfR）的含量，同时测量身高、体重等指标。结果：贫血孕妇的血清Fe、Cu、SF含量显低于非贫血孕妇，而血清锌、s-TfR含量两组差异无显性。结论：孕妇贫血不仅与缺铁有关，同时伴有铜等微量元素的缺乏。     

锌缺乏对孕鼠及其胎鼠体内元素分布的影响

为了解锌缺乏对妊娠大鼠及胎鼠体内元素分布的影响 ,将Wistar妊娠大鼠分为缺锌组、对喂组、补锌组和对照组 ,分别喂饲缺锌 (0 7mg kg)和正常锌 (10 0mg kg)饲料 ,在妊娠第 2 1天时处死孕鼠 ,取其血液、肝、脾、肾、胎盘和胎鼠 ,用原子吸收分光光度法测定锌、铜、铁、锰、钙含量。结果表明 ,缺锌组孕鼠各组织中锌和其他元素含量均显著低于补锌组和对照组 ;而且其血液、肝、脾、肾脏中铜、铁、锰含量显著低于对喂组 ,说明锌和其他元素在肠道吸收和组织分布方面存在协同关系 ,锌缺乏所致的动物摄食量减少不是引起组织中元素含量降低的主要原因。缺锌组胎盘中铁和胎鼠中铁、钙含量则显著高于其他三组 ,反映了锌与铁元素在胎盘可能存在竞争性转运。提示锌缺乏的母体和胎儿各元素在组织中分布不一致。