Zinc supplementation to protein-deficient diet in CO-exposed mice decreased fetal mortality and malformtion

In developing countries, diet during pregnancy is frequently low in both protein and zinc contents and exposure to CO is common because of environmental pollution and smoking. This study was conducted to evaluate whether zinc supplementation ameliorates fetal mortality and malformations in protein-deficient, CO-exposed mice. Pregnant mice of the CD-1 strain were maintained on 17% (reference) or 9% protein diets mixed with deficient, normal, or supplemental zinc throughout gestation. The dams in each dietary group were exposed to air (control) or 500 ppm CO in air in environmental chambers from gestation days 7–18. As compared to the control group (normal protein, normal zinc), the incidence of fetal mortality was 66.8% and 57.2% higher, respectively, and malformation incidence was 74.4% and 72.4% higher (0 and 500 ppm CO, respectively) in mice fed both deficient protein-zinc diets. However, the highest malformation rate was observed in the group with normal protein, deficient zinc (96% mortality in both 500 and 0 ppm CO, as compared to the reference group, p<0.0001). The fetal mortality rate was −3.5% (0 ppm CO) and 25.4% (500 ppm CO) lower in zinc-supplemented, protein-deficient groups compared to the control group. There was a significant negative association between fetal zinc concentrations and fetal malformations (p≤0.001). The result of this study might be relevant to populations that are exposed to CO and or consume marginal zinc and protein diets during gestation.     

Gastroschisis is caused by the combination of carbon monoxide and protein-zinc deficiencies in mice

BACKGROUND: Gastroschisis is a rare congenital defect of the abdominal wall. Its occurrence is noted primarily in the offspring of young mothers who often smoke during pregnancy. The incidence of gastroschisis has been increasing in many countries in recent years. The etiology of gastroschisis is not known. METHODS: Pregnant mice of CD‐1 strain were maintained on 17 and 9% protein diets mixed with deficient, normal, or supplemental zinc levels throughout gestation. The dams in each protein‐zinc diet group were randomly divided in two groups. One group was exposed to air (control) and the other to 500 ppm carbon monoxide (CO) in air, in environmental chambers, from gestation days (GD) 8–18. The dams were sacrificed by carbon dioxide asphyxiation on GD 18, and data on malformations was collected. RESULTS: The rates of fetal mortality and malformations were increased by protein and zinc deficiencies. Carbon monoxide exposure also increased fetal mortality. In the low protein group, the rate of fetal mortality was inversely related to the dietary zinc level, and the rate of fetal malformations was highest in the zinc deficient group. The incidence of gastroschisis in the low protein/zinc deficient/CO exposed group was 47%, and 60% of the litters were affected. The incidence of gastroschisis in the rest of the low protein/zinc diets/air or CO groups was 0. CONCLUSION: The data indicates that gastroschisis is caused by the combination of protein‐zinc deficiencies and carbon monoxide exposure during gestation. The finding may be relevant to human populations that experience protein and zinc deficiencies during gestation, and are exposed to CO pollution, or cigarette, or marijuana smoke during pregnancy. Birth Defects Res B 68:355–362, 2003. © 2003 Wiley‐Liss, Inc.     

Effects of zinc deficiency on morphogenesis of the fetal rat eye

Maternal zinc deficiency during pregnancy results in a high frequency of fetal eye malformations in the Long-Evans rat. In this study we examine the development of the eye from days 12 through 21 of gestation in conceptuses of dams fed deficient or adequate levels of zinc and also examine maternal plasma and conceptus zinc concentrations during this period. Dams were fed diets containing 0.5 (0.5 Zn group), 4.5 (4.5 Zn group), or 100 (100 Zn AL group) micrograms zinc per gram diet ad libitum, or 100 micrograms zinc g-1 diet in amounts restricted on a daily basis to the intake of matched animals from the 0.5 Zn group (100 Zn RI group). Conceptuses were removed and maternal plasma was collected on days 12, 14, 16, 19 and 21 of gestation. Maternal plasma and conceptus zinc concentrations reflected maternal dietary zinc level, with dam plasma Zn concentrations in the order of 0.5 Zn group less than 4.5 Zn group less than 100 Zn group on all days. A similar pattern held for embryo/fetus zinc, except for days 19 and 21, at which times the 0.5 Zn and 4.5 Zn fetuses had similar zinc concentrations. Histological examination of the developing eye of 0.5 Zn fetuses on days 12 and 14 revealed that invagination of the optic cup was often deficient, and that closure of the choroid fissure did not occur, resulting in colobomata and retinal folding visible at term. A very few fetuses were found at term to be anophthalmic or have only remnants of ocular tissue.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of dietary copper and zinc levels on tissue copper,zinc, and iron in male rats

The interaction between dietary copper and zinc as determined by tissue concentrations of trace elements was investigated in male Sprague-Dawley rats. Animals were fed diets in a factorial design with two levels of copper (0.5, 5 μg/g) and five levels of zinc (1, 4.5, 10, 100, 1000 μg/g) for 42 d. In rats fed the low copper diet, as dietary zinc concentration increased, the level of copper decreased in brain, testis, spleen, heart, liver, and intestine. There was no significant effect of dietary copper on tissue zinc levels. In the zinc-deficient groups, the level of iron was higher in most tissues than in tissues from controls (5 μg Cu, 100 μg Zn/g diet). In the copper-deficient groups, iron concentration was higher than control values only in the liver. These data show that dietary zinc affected tissue copper levels primarily when dietary copper was deficient, that dietary copper had no effect on tissue zinc, and that both zinc deficiency and copper deficiency affected tissue iron levels.     

Influence of low dietary calcium during pregnancy and lactation on zinc levels in maternal blood and bone in rats.

The effect of low dietary calcium on maternal zinc nutritional status was studied. Two groups of 6 adult female Wistar rats were fed during pregnancy and lactation with experimental diets containing either 0.2 g (LCa) or 0.6 g (NCa) of calcium/100 g. Both diets contained/100 g: 20.0 g protein (potassium caseinate), 3.5 mg Zn, 0.6 g P. A third group (n = 6) was fed a "stock diet" (SG), containing/100 g: 24.8 g protein, 1.5 g Ca, 0.6 g P, 11.6 mg Zn. Maternal blood samples were drawn from the tail before mating (To), at delivery (D) and at weaning (W); dams were sacrificed at weaning and the right femur was excised. Determinations (atomic absorption spectrometry) were: Zinc in red blood cells (RBC), Zn and Ca in ashed femur. The results (mean +/- SD) were: RBCZn (microg/mL) at To: 8.65 +/- 1.80, which did not change in the SG or in the NCa groups, but increased significantly in the LCa group (p < 0.001) (D: 18.20 +/- 4.63; W: 26.70 +/- 6.02), regarding To. Femur Zn (microg/100 mg) showed an increase (p < 0.001) in the LCa group (30.2 +/- 2.1) regarding both SG (25.3 +/- 0.7) and NCa groups (24.1 +/- 0.7). Femur Ca (mg/100 mg) decreased (p < 0.05) in the LCa group (19.2 +/- 0.9) regarding both SG (24.0 +/- 0.5) and NCa groups (21.4 +/- 0.7) and leading to a significant increase in Zn/Ca ratio (p < 0.001) in the LCa group. Therefore, dietary calcium deficiency during pregnancy and lactation would produce an increase of Zn utilization, reflected in the increase of maternal blood Zn levels and in femur Zn content.     

Gestational changes in concentrations of selenium and zinc in the porcine fetus and the effects of maternal intake of selenium

The effect of maternal dietary selenium (Se) and gestation on the concentrations of Se and zinc (Zn) in the porcine fetus were determined. Mature gilts were randomly assigned to treatments of either adequate (0.39 ppm Se) or low (0.05 ppm Se) dietary Se. Gilts were bred and fetuses were collected throughout gestation. Concentrations of Se in maternal whole blood and liver decreased during gestation in sows fed the low-Se diet compared to sows fed the Se-supplemented diet. Maternal intake of Se did not affect the concentration of Se in the whole fetus; however, the concentration of Se in fetal liver was decreased in fetuses of sows fed the low-Se diet. Although fetal liver Se decreased in both treatments as gestation progressed, the decrease was greater in liver of fetuses from sows fed the low-Se diet. Dietary Se did not affect concentrations of Zn in maternal whole blood or liver or in the whole fetus and fetal liver. The concentration of Se in fetal liver was lower but the concentration of Zn was greater than in maternal liver when sows were fed the adequate Se diet. These results indicate that maternal intake of Se affects fetal liver Se and newborn piglets have lower liver Se concentrations compared to their dams, regardless of the Se intake of sows during gestation. Thus, the piglet is more susceptible Se deficiency than the sow.     

Dietary zinc supplementation attenuates hyperglycemia in db/db mice

Although zinc (Zn) deficiency has been associated with insulin resistance, and altered Zn metabolism (e.g., hyperzincuria, low-normal plasma Zn concentrations) may be present in diabetes, the potential effects of Zn on modulation of insulin action in Type II diabetes have not been established. The objective of this study was to compare the effects of dietary Zn deficiency and Zn supplementation on glycemic control in db/db mice. Weanling db/db mice and lean littermate controls were fed Zn-deficient (3 ppm Zn; dbZD and InZD groups), Zn-adequate control (30 ppm Zn; dbC and InC groups) or Zn-supplemented (300 ppm Zn; dbZS and InZS groups) diets for 6 weeks. Mice were assessed for Zn status, serum and urinary indices of diabetes, and gastrocnemius insulin receptor concentration and tyrosine kinase activity. Fasting serum glucose concentrations were significantly lower in the dbZS group compared with the dbZD group (19.3 +/- 2.9 and 27.9 +/- 4.1 mM, respectively), whereas the dbC mice had an intermediate value. There was a negative correlation between femur Zn and serum glucose concentrations (r = -0.59 for lean mice, P = 0.007). The dbZS group had higher pancreatic Zn and lower circulating insulin concentrations than dbZC mice. Insulin-stimulated tyrosine kinase activity in gastrocnemius muscle was higher in the db/db genotype, and insulin receptor concentration was not altered. In summary, dietary Zn supplementation attenuated hyperglycemia and hyperinsulinemia in db/db mice, suggesting that the roles of Zn in pancreatic function and peripheral tissue glucose uptake need to be further investigated.     

Inducibility and amounts of metallothionein as influenced by cadmium and zinc in the developing rat

Information on the accumulation and/or depletion of Zn in metallothionein (MT) of rat fetus, rat pup, and maternal rat liver at various ages was obtained with pregnant rats fed a basal casein diet or this diet plus either 100 ppm Zn or 50 ppm Cd. Rats fed each of the respective diets were sacrificed on 12, 16, and 20 d of gestation and 0, 7, 14, and 28 d post-partum. No Cd was detected in the placenta or fetal tissue and the Cd did not affect the accumulation of Zn in the fetal MT, but it did increase the Zn content in liver MT of the dams. Very little Zn in MT was found on day 12 of gestation, but Zn rapidly increased in MT to a maximum at time of birth. The accumulation of Zn in MT was independent of the diet for the fetuses, but the Zn accumulation in the dam and pup tissues was diet dependent. In order to study age-dependent difference in the inducibility of MT, newborn, 5-week-old, or 24-week-old rats were injected with zinc at the levels of 0, 3, 6, or 9 mg/kg and 5 h later injected with³⁵S-cystine. In rats sacrificed 1 h later, the amount of radioactivity in liver MT demonstrated that this protein in older animals was more readily induced by Zn than in younger animals.     

Relationship of dietary zinc to 6-mercaptopurine teratogenesis and DNA metabolism in the rat

The possible interaction between the level of maternal dietary zinc and the teratogenic activity of 6-mercaptopurine was investigated. Pregnant Sprague-Dawley rats were fed diets containing 9,100 or 1,000 ppm zinc from day zero of pregnancy and were given a single intraperitoneal injection of 6-MP (55mg/kg) on day 11. At term, females in the group fed 1,000 ppm zinc (a high intake) showed less pronounced effects on reproduction and embryogenesis than did those fed 9 ppm (marginally deficient) or 100 ppm (normal) zinc. Embryos examined on day 12 of gestation had similar concentrations of protein and RNA; however, the DNA content was lower and the incorporation of 3H-thymidine was greater in the drug treated groups than in non-drug treated controls. These results indicate that 6-mercaptopurine is acting to alter embryonic DNA metabolism and that high levesl of dietary zinc may ameliorate some of the deleterious effects of this drug on embryonic and maternal toxicity.     

Regulation of the ontogeny of rat liver metallothionein mRNA by zinc

To investigate the role of metals in the regulation of the ontogenic expression of rat liver metallothionein (MT) mRNA, the concentrations of zinc, MT and MT mRNA were determined in livers of fetal and newborn rats from dams which were fed with a control or zinc-deficient or copper-deficient or iron-deficient diet from day 12 of gestation. The liver samples were analyzed for MT-mRNA levels using a mouse MT-I cRNA probe. Although the newborn hepatic levels of each metal (zinc or copper or iron) was specifically reduced corresponding to the respective mineral deficiencies, the hepatic concentrations of total MT and MT-I mRNA were significantly decreased only in pups born from zinc-deficient dams. Injection of the zinc-deficient newborn pups with 20 mg Zn as ZnSO4/kg restored with MT-I mRNA levels to slightly above control values within 5 h of injection. The hepatic zinc, MT and MT-I mRNA levels were observed to increase significantly in control fetal rat liver on days 17-21 of gestation but there were little changes in either zinc or MT in fetal livers from zinc-deficient dams during the late gestational period. The MT-I mRNA level also did not show an increase on days 18 and 20 of gestation in zinc-deficient fetal liver as compared to controls. These results demonstrate a direct role of zinc in hepatic MT gene expression in rat liver during late gestation. Immunohistochemical localization of MT using a specific antibody to rat liver MT showed that the staining for MT in zinc-deficient pup liver was mainly in the cytosol in contrast to the significant nuclear MT staining observed in control newborn rat liver. The results suggest that maternal zinc deficiency has a marked effect not only in decreasing the levels of hepatic MT and MT-I mRNA but also in the localization of MT in newborn rat liver.     

Dietary zinc deficiency decreases plasma concentrations of vitamin E

Experiments were conducted to examine the effects of dietary zinc (Zn) upon plasma vitamin E (E) concentrations to test the hypothesis that there may be a significant dietary interaction between these two nutrients. Weanling female Sprague-Dawley rats were fed diets that were (i) Zn-deficient (less than 0.9 micrograms Zn/g diet) ad libitum; (ii) Zn-adequate (50.9 micrograms Zn/g diet), pair-fed to the Zn-deficient group; and (iii) Zn-adequate (50.9 micrograms Zn/g diet) ad libitum. Plasma E in Zn-deficient animals (4.02 +/- 1.20 micrograms/ml) was significantly reduced (P less than or equal to 0.05) compared with results in both Zn-adequate pair-fed (9.21 +/- 0.70 micrograms/ml) and Zn-adequate ad libitum-fed (9.47 +/- 0.90 micrograms/ml) animals. Zn deficiency in this model system also resulted in significant (P less than or equal to 0.05) reductions in femur and plasma Zn concentrations as well as in plasma retinol, plasma triglyceride, and plasma cholesterol concentrations. Plasma albumin and total plasma protein concentrations were normal in Zn-deficient animals. With dietary Zn deficiency, the decrease in plasma E appeared to be out of proportion to associated decreases in plasma triglyceride and plasma cholesterol concentrations. Since E is associated with plasma lipoproteins, these data suggest that lipid and/or E malabsorption may be a consequence of Zn deficiency. In response to increased dietary intake of E, increments of plasma E were lower in Zn-depleted than in Zn-adequate, pair-fed animals. These findings suggest that dietary Zn deficiency possibly may increase the nutritional requirement for E necessary to maintain adequate plasma concentrations.     

The effect of magnesium and manganese uptake and accumulation on oxygen consumption and ammonia excretion in Porcellio spinicornis Say (Porcellionidae, Isopoda)

Mean concentrations of Mg and Mn in whole intermoult 7th growth-stage Porcellio spinicornis are positively correlated with dietary levels up to and including 1,000 ppm of these two trace metals. Lower tissue concentrations in isopods on 1,500 ppm diets are related to either a low food intake or a higher rate of metal excretion. Mean Mg concentration in whole isopods at the end of 7 days ranged from 27 388.26 +/- 598.56 micrograms/g dry tissue in the control to 69 122.08 +/- 31 682.98 micrograms/g dry tissue in the 1,000 ppm dietary group; in the 1,500 ppm dietary group, it amounted to 25 630.26 +/- 13 102.12 micrograms/g dry tissue. Mean Mn concentration varied from 85.53 +/- 11.23 micrograms/g dry tissue in the control to 229.05 +/- 32.33 micrograms/g dry tissue in 1,000 ppm dietary group; in the 1,500 ppm dietary group, it amounted to 199.57 +/- 18.99 micrograms/g dry tissue. Differences between the two sexes were significant at 5% level. Oxygen consumption was negatively and ammonia excretion was positively related to the dietary metal concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)     

The effect of various dietary zinc concentrations on the biological interactions of zinc,copper, and iron in rats

Three groups (14 rats each) were fed one of the following diets for 8 wks: a control purified basal diet containing 12 ppm zinc, 5 ppm copper, and 35 ppm iron; the basal diet with less than 2 ppm zinc; or the basal diet supplemented with 1000 ppm zinc. Rats fed the zinc-deficient diet had decreased weight gain, moderate polydipsia, and intermittent mild diarrhea. The zinc-supplemented rats had a cyclical pattern of food intake and weight loss from weeks 5 to 8. Tissue concentrations suggest that zinc and copper were not mutually antagonistic with chronic dietary imbalances. If tissue element concentrations reflected intestinal uptake, then competition and/or inhibition of intestinal uptake occurred between zinc and iron. The fluctuations in tissue element concentrations that occurred with increased duration of the study were at variance with previous studies of shorter time periods. The dietary proportions of zinc, copper, and iron appear to influence zinc, copper, and iron metabolism at the intestinal and cellular transport levels over a given period of time.     

Zinc availability and digestive zinc solubility in piglets and broilers fed diets varying in their phytate contents, phytase activity and supplemented zinc source

The study was conducted to evaluate the effects of dietary zinc addition (0 or 15 mg/kg of Zn as inorganic or organic zinc) to three maize-soybean meal basal diets varying in their native Zn, phytic P contents and phytase activity (expressed in kg of feed: P- with 25 mg Zn and 1.3 g phytic P, P+ with 38 mg Zn and 2.3 g phytic P or P+/ENZ being P+ including 500 units (FTU) of microbial phytase per kg) in two monogastric species (piglets, broilers). Measured parameters were growth performance, zinc status (plasma, and bone zinc) and soluble zinc in digesta (stomach, gizzard and intestine). The nine experimental diets were fed for 20 days either to weaned piglets (six replicates per treatment) or to 1-day-old broilers (10 replicates per treatment). Animal performance was not affected by dietary treatments (P > 0.05) except that all P- diets improved body weight gain and feed conversion ratio in piglets (P < 0.05). Piglets fed P- diets had a better Zn status than those fed P+ diets (P < 0.05). In both species, Zn status was improved with supplemental Zn (P < 0.05), irrespective of Zn source. Phytase supplementation improved piglet Zn status to a higher extent than adding dietary Zn, whereas in broilers, phytase was less efficient than supplemental Zn. Digestive Zn concentrations reflected the quantity of ingested Zn. Soluble Zn (mg/kg dry matter) and Zn solubility (% of total Zn content) were highest in gizzard contents, which also presented lower pH values than stomach or intestines. The intestinal Zn solubility was higher in piglet fed organic Zn than those fed inorganic Zn (P < 0.01). Phytase increased soluble Zn in piglet stomach (P < 0.001) and intestine (P = 0.1), but not in broiler gizzard and intestinal contents. These results demonstrate (i) that dietary zinc was used more efficiently by broilers than by piglets, most probably due to the lower gizzard pH and its related higher zinc solubility; (ii) that zinc supplementation, irrespective of zinc source, was successful in improving animal's zinc status; and (iii) suggest that supplemented Zn availability was independent from the diet formulation. Finally, the present data confirm that phytase was efficient in increasing digestive soluble Zn and improving zinc status in piglets. However, the magnitude of these effects was lower in broilers probably due to the naturally higher Zn availability in poultry than in swine.     

Bioavailability of zinc and its binding to casein in milks and formulas

Differences in zinc bioavailability among milk and formulas may be attributed to binding of zinc to various ligands. We determined the distribution of zinc and protein at different pHs and zinc and calcium concentrations. We used radiolabelled cow's milk, human milk, whey-predominant (WPF) and casein-predominant (CPF) infant formula. Lowering the pH changed zinc and protein distribution: zinc shifted from pellet (casein) to whey in cow's milk, from fat to whey in human milk and from fat and pellet to whey in formulas. Protein shifted from whey to pellet in human milk and from whey and pellet to fat in formulas. Increasing zinc and calcium concentrations shifted protein and zinc from pellet to whey for cow's milk and from whey and pellet to fat for the formulas. Protein distribution was not affected by calcium or zinc addition in human milk or CPF, while zinc shifted from whey to fat in human milk and from fat and pellet to whey in CPF. Zinc and calcium binding to isolated bovine or human casein increased with pH. At 500 mg/L of zinc, bovine casein bound 32.0 +/- 1.8 and human casein 10.0 +/- 0.9 mg zinc/g protein. At 500 mg/L of calcium, calcium was preferentially bound over zinc. Adding calcium and zinc resulted in 32.0 +/- 1.8 mg zinc/g bound to bovine casein and 17.0 +/- 0.8 mg zinc/g to human casein, while calcium binding was low. Suckling rat pups dosed with 65Zn labelled infant diets were killed and individual tissues were gamma counted. Lower zinc bioavailability was found for bovine milk at pH = 4.0 (%65Zn in liver = 18.7+1.4) when compared to WPF (22.8 +/- 1.6) or human milk (26.9 +/- 0.8). Lowering the pH further decreased zinc bioavailability from human milk, but not from cow's milk or WPF. Knowledge of the compounds binding minerals and trace elements in infant formulas is essential for optimizing zinc bioavailability.     

Gestational zinc deficiency amplifies the regulation of metallothionein induction in adult mice

To determine if prenatal zinc deficiency has a persistent effect on metallothionein (MT) regulation, Swiss-Webster mice were mated and fed a diet containing either control (100 micrograms Zn/g) or low levels of zinc (5 micrograms Zn/g) from Day 7 of gestation to parturition. After birth all mice were given the control diet. Liver zinc and MT levels were 50% lower in newborn pups from dams fed the low zinc diets than in control pups. In control pups, liver zinc and MT concentrations were relatively stable during the first week of postnatal life. In contrast, in pups prenatally deprived of zinc, liver levels of zinc and MT increased such that by Day 3 of postnatal life, the levels were not significantly different from controls. At Day 56, serum IgM concentrations were significantly lower in the low zinc offspring. Liver zinc concentrations in the two groups of mice were similar at Day 70 postnatal, and in both groups liver MT levels were below detection limits. However, when Day 70 mice were given zinc injections to stimulate MT synthesis, the prenatally zinc deprived offspring showed markedly higher liver MT levels than did control mice given similar injections, despite similar liver zinc concentrations in the two groups. These results show that prenatal zinc deficiency has pronounced effects on postnatal MT metabolism which can persist into adulthood.     

Erythrocytary zinc and the infant growth profile in northeast Brazil

This study evaluated nutritional status linked to zinc levels in 239 randomly selected children at crèches in Teresina, Brazil, aged 3 to 6. Blood samples were collected after fasting of 10 h. Erythrocytary zinc levels were determined through flame atomic absorption spectrophotometry. Zinc deficiency was determined as below 40 microg Zn/g Hb. Infant linear growth was evaluated measuring weight and height, and nutritional status by height/age, weight/height, and weight/age indices, expressed as Z scores, in line with the National Center for Health Statistics. The mean zinc concentration was 35.50 +/- 10.95 microg Zn/g Hb. Zinc distribution in the 10, 50, 75, and 90 percentiles was 24.73 microg Zn/g Hb, 35.45 microg Zn/g Hb, 40.73 microg Zn/g Hb and 52.77 microg Zn/g Hb, respectively. Based on this distribution, normal values were found only from the 75th percentile and above. Since the cutoff point adopted was 40 microg Zn/g Hb, the prevalence of zinc deficiency was 74.3%. As for growth profile, 8.4% were chronically malnourished, although the statistical association between linear impairment and nutritional status regarding zinc was insignificant. The study revealed that an important segment of the infant population was mineral deficient; however, the degree of deficiency did not influence growth profiles.     

Threshold for carbon monoxide induced fetotoxicity

Carbon monoxide (CO) is said to be the most widely encountered occupational and environmental contaminant. Threshold for CO-induced fetotoxicity was studied using mouse as an experimental animal. Pregnant animals of CD-1 strain were exposed to 0, 65, 125, 250, or 500 ppm CO from gestation day 7 to 18. The animals were sacrificed on gestation day 18, and their uterine horns were examined for live or resorbed fetuses. The data suggest that maternal CO exposure to as low as 125 ppm affects fetal growth and higher levels affect viability. The data also suggest that the developing organism is sensitive to chronic CO exposure, and this sensitivity is dose dependent. The fetal mouse is influenced at levels of exposure below those found transiently for human cigarette smokers and ambient CO concentrations associated with various occupations.     

Prevalence of zinc deficiency in junior high school students of Tehran City

Zinc deficiency is a health problem in many communities especially among adolescents because of pubertal growth sprout. This investigation was carried out to determine the epidemiology of zinc deficiency in junior high school students in Tehran City in 1997. This cross-sectional study was performed on 881 students (452 males and 429 females) with the mean age of 13.2±1.0 yr, who were selected by multistage random sampling method. Plasma, erythrocyte, and hair zinc levels were assayed by flame atomic absorption spectrophotometry. Anthropometric and demographic characteristics were measured and recorded on a questionnaire. Dietary intakes were evaluated by a 24-h recall method. Zinc deficiency was defined as having at least two indices from indices of erythrocyte, plasma, and hair zinc below 10 μg/mL, 100 μg/dL, and 125 μg/g of hair, respectively. The results showed that zinc deficiency prevalence was 31.1% (confidence interval: 28–34.4%). Zinc deficiency was 65%, 49%, and 1.3% based on plasma, erythrocyte, and hair zinc levels, respectively. The mean ± SD for plasma, erythrocyte, and hair zinc concentration, height-for-age, as well as weight-for-age Z scores were 95.2±17.7 μg/dL, 10.3±2.3 μg/mL, 239.4±54.4 μg/g, −0.40±0.92, and 0.12±0.91, respectively. As for dietary intake compared with the RDA, 50% of the subjects consumed less than 50% of their requirement for zinc RDA based on a 24-h dietary recall. Zinc intake in subjects was 7.5±3.7 μg, that in boys was higher than in girls. Correlation coefficients between zinc status indices were very weak. There was neither a linear nor nonlinear relationship between biochemical parameters and nutritional zinc intake. It is concluded that almost one-third to one-half of the subjects would be considered zinc deficient.     

Interaction of maternal protein and carbon monoxide on pup mortality in mice: implications for global infant mortality

BACKGROUND: The United States Surgeon General declared 2005 as the "Year of Healthy Child." To improve the health of all children, we need to start before pregnancy, with their mothers. Unfortunately, protein deficiency in the diets of poor pregnant mothers in developing countries is widespread. Carbon monoxide (CO) pollution is serious public health problem in developed and developing countries. METHODS: A two-way factorial experimental design was used. Mice were maintained on 27%, 16%, 8%, or 4% protein diets. Dams were exposed to 0 ppm (control), 65 ppm, or 125 ppm CO in air, in environmental chambers for 6 hr/day during the first 2 weeks of pregnancy. Controls were also subjected to environmental chamber conditions. Food and water were available at all times. Animals were allowed to deliver, and data on pup mortality was recorded. RESULTS: Litter size was not affected by CO exposure, but was directly related to the dietary protein levels. Pup weight was inversely related to the CO exposure level, and directly related to the dietary protein levels. Pup mortality on date of birth was increased by CO exposure and was inversely related to the dietary protein levels. Pup mortality at 1 week of age was increased by CO exposure and 55% of all pups died in 125 ppm CO exposed group. Pup mortality at 1 week of age was inversely related to dietary protein levels. All pups in the 4% dietary protein and in all concentrations of CO died. All pups in the 8% protein group and in all CO concentrations died except in 125 ppm CO group. Pup mortality in the 16% dietary protein group ranged from 14.8% in 0 ppm to 36.8% in 65 ppm CO groups. Pup mortality in the 27% dietary protein group ranged from 14.3% in the 0 ppm to 41.1% in the 125 ppm CO groups. CONCLUSIONS: DATA suggest that protein deficiency and CO exposure enhance pup mortality. The protein and CO also interact to increase pup mortality in 16% and 27% protein groups. Carbon monoxide exposure, along with protein deficiency during gestation, may be contributing factors for high rates of infant mortality in developing countries. The results of the study also suggest that un-vented combustion for heating and cooking, ambient pollution, and biomass smoke may have a major impact on the health of children worldwide; and may explain the causes of high infant mortality in poor countries and some sections of the United States population.