Effect Of Zinc Deficiency Research Articles

Effect of zinc deficiency on thyroid hormone synthesis and thyroid antibodies

Effect of zinc deficiency on thyroid hormone synthesis and thyroid antibodies

Effect of zinc deficiency on hepatic protein expression patterns in rats

Zinc deficiency is an important public health problem in the world. Zinc deficiency causes metabolic abnormalities, probably in part due to the altered protein expression patterns. This study was aimed to investigate hepatic protein expression patterns in zinc deficient rats. Thirty 3-week-old male Sprague-Dawley rats were randomly divided into three groups and fed the respective diet for four weeks. The ad libitum-fed control group (CON) and the pair-fed group (PF) were given AIN-93G diet, and zinc-deficient group (ZD) was given zinc-deficient diet (zinc level 4.5 mg/kg). After dietary regimen, liver was excised under ethylether anesthesia and stored at −80 degree until analyses. Liver homogenate was subjected to 2-D PAGE. Gels were digitally scanned and intensity of protein spots was statistically analyzed by principal component analysis. The first and second components (PC1 and PC2) explained 45% and 32% of all variance, respectively. PC1 was significantly different among all three groups (P<0.001 by Fisher's PLSD). ZD was placed between CON and PF in terms of PC1. PC2 of ZD was significantly different from that of CON and PF (P<0.001), while PC2 was almost identical between CON and PF. These results suggest that PC1 is related to the response to diet restriction, and PC2 is related to zinc deficiency per se. Supported by Japan Society for the Promotion of Science Grants-in-Aid for Scientific Research (C) (22500772).

破骨細胞分化因子（RANKL）と，その受容体RANKの発現に及ぼす亜鉛欠乏の影響

破骨細胞分化因子（RANKL）と，その受容体RANKの発現に及ぼす亜鉛欠乏の影響

Effects of Zinc Deficiency on Colonic Microbiota

The purpose of this study was to evaluate colonic microbiota composition in response to a dietary zinc deficiency in mice. Male, 12‐wk‐old CD‐1 mice (n=5/ diet group) were fed a zinc adequate (ZA, 30.0 ppm) or a zinc deficient (ZD, 0.85 ppm) diet for 4 weeks. Transcript levels of colonic metallothionein (MT) and the zinc transporter (Zip4) were measured by qPCR as markers of zinc status. MT mRNA levels decreased by 0.55 fold (p=0.032) while Zip4 mRNA levels increased 2.88 fold (p=0.016). ZD mice didn't experience weight loss normally associated with deficiency. However, there was a difference in weight gain (6.9%± 1.6 vs. 3.6%± 1.1, p=0.01) in ZA and ZD mice, respectively. Microbiota composition was analyzed by denaturing gradient gel electrophoresis (DGGE) analysis and 16S rRNA sequencing. Initial DGGE profiling suggested that ZA and ZD groups differed in intestinal microbiota composition. 454 based 16S rRNA sequencing identified various phylotypes that, at the level of 99% identity, showed significant differences (p≤0.05) between the two diet groups. Weighted UniFrac analysis of overall microbiota composition indicated that ZD grouped separately from ZA, suggesting that a 4‐week zinc deficient diet alters overall colon microbiota composition in mice. Sponsored by the University of Florida University Scholars Program

Effect of zinc deficiency on memory, oxidative stress and blood chemistry in rats

The effect of zinc deficiency on memory function, oxidative stress and blood chemistry in rats was investigated. Forty-two male (65.0±2.78 g) albino Sprague Dawley rats were equally divided into 3 groups, A, B and C. The 3 groups of rats were fed zinc deficient diet, zinc adequate diet and reference diet, respectively, and water ad libitum daily for 30 days. Body weight, feed and water intake of the rats were computed every day. A shuttle box was used for the short-term and long-term memory tests of these rats fed the respective diets. Two criteria were considered as behavioural test; these include latency in entering dark chamber and timespent in the light chamber before entering the dark chamber at days 2, 9, 16 and 23 after the first day of training using the shuttle box. After the memory testing was conducted, rats were sacrificed by decapitation, blood was taken and brain excised. Total brain protein, plasma creatinine, reduced glutathione (GSH) levels, specific activities of acetylcholinesterase, superoxide dismutase (SOD), aspartate aminotransferase (AST), alanineaminotransferase (ALT) and alkaline phosphatase (ALP) were determined. The control diet supported significantly (p

The Effect of Severe Zinc Deficiency and Zinc Supplement on Spatial Learning and Memory

Zinc deficiency during pregnancy and during lactation has been shown to impair cognitive function and motor activity in offspring rats. In the present study, the effect of zinc deficiency and zinc supplement on spatial learning and memory in Morris Water Maze (MWM) and motor activity in open field were investigated. Pregnant rats after mating were divided to three groups. Control group fed a standard diet and a zinc deficient (ZnD) group fed a diet deficient in zinc (0.5-1.5 ppm) and a zinc supplement (ZnS) group fed a standard diet and enhanced zinc in the drinking water (10 ppm). All the diets were exposed during the last trisemester of pregnancy and during lactation. Rat's offspring in these groups were tested for spatial learning and memory in MWM at post natal day (PND) 56 and were tested for motor activity in open field at PND 66.The Escape Latency (EL) and Traveled Distance (TD) in the ZnD group were increased but Percentage of Time Spent in the target quadrant (PTS) was decreased compared to the control group. In addition, these were no significant differences in EL and TD, but PTS had significant increase in ZnS compared to the control group. In the open field, Total Distance Moved (TDM) and Time of Motor Activity (TMA) for the ZnD were decreased compared to the control group, but there were no significant differences in TDM and TMA between control and ZnS groups. These findings suggest that zinc deficiency during the last trimester of pregnancy and during lactation impaired spatial learning and memory in their offsprings and has also negative effect on motor activity. In addition, ZnS has a significant effect on spatial learning and memory but no effect on motor activity in their offsprings.

Zinc-Deficiency Induced Changes in the Distribution of Rat White Blood Cells

Zinc is known to play an important role for immune-functions. However, the effects of zinc-deficiency on the immune response system from the point of view of the distribution changes of the number of total white blood cells (WBCs) are still primarily unknown. Therefore, the effects of zinc-deficiency on the number of total WBCs, neutrophil, eosinophil, basophil, monocyte and lymphocytes (T lymphocyte, B lymphocyte and NK cell) were studied in rats. The weaned male rats were randomly divided into the zinc deficient diet (ZDD: 0.7 mg zinc/kg diet) group and the control diet (CON: 34.8 mg zinc/kg diet) group, and were pair-fed for 4 wk. The number of lymphocyte subsets, visceral organ weights, serum zinc, corticosterone and IL-6 concentrations were also determined. Zinc-deficiency increased duration-dependently the number of total white blood cells, granulocytes (neutrophil, eosinophil and basophil) and monocytes in 2-4 wk without changing the number of lymphocytes, T lymphocytes, B lymphocytes or NK cells. The relative weights of thymus and adrenals were 0.63 times (p<0.01) lower and 1.60 times (p<0.001) higher in ZDD group than in CON group, respectively. Zinc-deficiency increased serum corticosterone concentration to 1.48 times (p<0.05) without changing serum IL-6 concentration, as compared with those of CON group. From these results, zinc-deficiency increases markedly the number of granulocytes and monocytes without changing the number of lymphocytes, T lymphocytes, B lymphocytes or NK cells. These results also suggest that zinc-deficiency induces stress responses and the responses may have in part participated in increased actions of the number of granulocytes and monocytes during zinc-deficiency, and induce thymus atrophy and adrenal hypertrophy.

Effect of Zinc Deficiency on Haematological Parameters and Mineral Contents of Selected Tissues in Albino Rats

The effect of zinc deficiency on tissue level of some minerals (Na, K, Ca, P, Cu, Fe, Mg, Zn, Mn) in growing rats was investigated. Two groups of rats were fed either a zinc adequate diet or zinc deficient diet (6 ppm) for six weeks. At the end of the feeding period, zinc deficiency decreased the final body weight of the rats by 70% compared to the control. There was no significant difference (P < 0.05) in the packed cell volume (PCV) and the white blood cell count (WBC) of the zinc deficient rats was significantly increased (P < 0.05) compared to the control. Tissue content of minerals measured in the liver and kidney of both group of rats showed that zinc deficiency significantly increased (P < 0.05) tissue concentration of some elements (Fe, Cu, Ma, Ca, K and Na) while Mg and phosphorus levels were lowered compared to the control. This result suggest that zinc deficiency in rats could have adverse effect on intermediary metabolism as a result of interplay in the interactions between these minerals.

Effects of zinc deficiency on DNA damage, oxidative stress and oxidant defense in peripheral blood of rats

Approximately 12% of Americans do not consume the EAR for zinc and could be at risk for marginal zinc deficiency. There is accumulating evidence that zinc deficiency is associated with increased risk of cancer mortality and increased DNA damage in vitro. We hypothesize that zinc deficiency in vivo causes DNA damage through increases in oxidative stress and compromised oxidant defense. To test this hypothesis, SD rats were fed an adequate zinc diet (MZA 30ppm) or marginal zinc deficient diet (MZD 6ppm) for 6 weeks. Comet assay revealed a significant increase in DNA damage in peripheral blood cells of MZD rats. Oxidative stress was also increased as indicated by alterations in plasma F2‐isoprostanes. However, no changes in plasma total antioxidant capacity, ascorbic acid, α–tocopherol, and erythrocyte SOD activity were found with MZD. We also investigated the effects of severe zinc deficiency with repletion on DNA damage. Rats were fed an adequate zinc (30ppm), zinc deficient (&lt;1ppm), or pair‐fed diet for 3 weeks prior to 1 week zinc repletion. DNA damage of peripheral blood cells was significantly increased after zinc depletion, but reversed back to normal levels after zinc repletion. These data suggest interactions among zinc deficiency, DNA integrity and oxidative stress and implicate the role of zinc deficiency in cancer susceptibility.

Acetaldehyde addition throughout the growth phase alleviates the phenotypic effect of zinc deficiency in Saccharomyces cerevisiae

During experiments to determine the effects of exogenously added acetaldehyde on pure cultures of various yeast strains, we discovered that an early acetaldehyde perfusion during the growth phase allowed several yeasts to partially overcome the phenotypic effects of zinc depletion during alcoholic fermentation. We, therefore, performed genome-wide expression and proteomic analysis on an industrial Saccharomyces cerevisiae yeast strain (VL1) growing in zinc-replete or zinc-depleted conditions in the presence of perfused acetaldehyde to identify molecular markers of this effect. Zinc depletion severely affects ethanol production and therefore nicotinamide adenine dinucleotide (NAD) regeneration, although we observed partial compensation by the upregulation of the poorly efficient Fe-dependent Adh4p in our conditions. A coordinate metabolic response was indeed observed in response to the early acetaldehyde perfusion, and particularly of the lower part of glycolysis, leading to the cellular replenishment of NAD cofactor. These various findings suggest that acetaldehyde exchange between strains may inhibit the growth of some yeast strains while encouraging the growth of others. This phenomenon could be particularly important for understanding the ecology of colonization of complex fermentation media by S. cerevisiae after elimination of non-Saccharomyces yeasts.

Zinc deficiency reduces paclitaxel efficacy in LNCaP prostate cancer cells

Chemotherapeutics used to treat prostate cancer are often from a class of drugs that target microtubule networks, such as paclitaxel. A previous report indicated that supplemental zinc sensitized prostate cancer cells to paclitaxel-induced apoptosis, suggesting that increased zinc levels might enhance paclitaxel efficacy. The effect of zinc deficiency on paclitaxel activity is not known though, so we tested this in two prostate cancer cell lines maintained under moderately zinc-deficient conditions. LNCaP and PC3 cell lines were used as models of early and late-stage prostate cancer, respectively. Cells cultured in reduced zinc levels did not demonstrate altered cell viability, growth rates, or intracellular zinc content. Additionally, zinc deficiency alone had no apparent effect on cell cycle kinetics or apoptosis levels. However, the IC 50 for paclitaxel-induced cell cycle arrest increased in LNCaP cells from zinc-deficient compared to zinc-replete conditions. Consequently, paclitaxel-induced apoptosis was reduced in LNCaP cells from zinc-deficient compared to zinc-replete conditions. In PC3 cells, the effects of paclitaxel were independent of zinc status. Reduced extracellular zinc levels were shown to affect paclitaxel activity in a prostate cancer cell line. Given the prevalence of zinc deficiency, determining how chemotherapeutic action is modulated by zinc adequacy may have clinical importance.

Effects of Zinc Deficiency and Drought on Plant Growth and Metabolism of Reactive Oxygen Species in Maize ( Zea mays L)

Abstract The combinative effects of applied zinc (Zn) and soil moisture on the plant growth, Zn uptake, and the metabolism of reactive oxygen species (ROS) in maize ( Zea mays L.) plants were examined through two pot experiments under greenhouse conditions. Maize variety Zhongdan 9409 was used. In experiment 1, maize plants were grown in cumulic cinnamon soil with five Zn treatments (0, 3.0, 9.0, 27.0, and 81.0 mg Zn kg -1 soil). Three treatments of soil moisture including serious drought, mild drought, and adequate water supply were set at 30-35%, 40-45%, and 70-75% (w/w) of soil saturated water content, respectively. Soil saturated water content was 36% (w/w). The dry matter weights of shoots were enhanced by Zn application and adequate water supply. There was no apparent difference in plant growth among Zn application rates from 3.0 to 81.0 mg Zn kg -1 soil. The increases of plant growth and Zn uptake due to Zn application were found more significant under well-watered condition than under drying condition. In experiment 2, two levels of Zn (0 and 5.0 mg Zn kg -1 soil) and soil moisture regimen (40-45% and 70-75% of soil saturated water content, respectively) were set. Zn deficiency or water stress resulted in higher concentrations of O 2 − · and malondiadehyde in the first fully expanded leaves. Zn deficiency lowered the activity of superoxide dismutase (SOD, EC 1.15.1.1) in leaves. Drought stress increased SOD activity in leaves regardless of Zn supply. The activity of guaiacol peroxidase (POD, EC1.11.1.11) was found to be enhanced by Zn supply only in well-watered leaves. Zinc deficiency or water stress had little effect on the activity of catalase (CAT, EC 1.11.1.6). The higher ROS level in early maize leaves due to water stress seemed not to be alleviated or lowered partially by Zn application. However, Zn fertilizer was recommended to apply to maize plants irrigated or supplied with adequate water, otherwise Zn deficiency would reduce the water use for plant biomass production.

Influence of iron and zinc status on cadmium accumulation in Bangladeshi women

Cadmium is a widespread environmental contaminant present in food. The absorption in the intestine increases in individuals with low iron stores, but the effect of zinc deficiency is not clear. The aim of the present study was to assess the influence of iron and zinc status on cadmium accumulation in pregnant Bangladeshi women. We measured cadmium in urine from 890 women using inductively coupled plasma mass spectrometry (ICPMS). Further, we also measured ferritin and zinc in plasma. The median cadmium concentration in urine was 0.59 μg/L (adjusted to mean specific gravity of 1.012 g/mL). Analysis of covariance (ANCOVA) showed that urinary cadmium was associated with plasma ferritin and plasma zinc via a significant interaction between dichotomized plasma ferritin and plasma zinc. The analysis was adjusted for age and socioeconomic status. Women with low iron stores and adequate zinc status had significantly higher urinary cadmium compared to women with both adequate iron stores and zinc status. There was no difference in urinary cadmium between women with both low iron stores and zinc status compared to those with both adequate iron stores and zinc status. In conclusion, low iron stores were associated with increased cadmium accumulation, but only at adequate zinc status.

Effects of zinc deficiency on the number of white blood cells in rats

Effects of zinc deficiency on the number of white blood cells in rats

Effects of Zinc Deficiency and Drought on Grain Yield of Field‐grown Wheat Cultivars in Central Anatolia

AbstractDrought stress and zinc (Zn) deficiency are serious abiotic stress factors limiting crop production in Turkey, especially in Central Anatolia. In this study, the effects of Zn deficiency and drought stress on grain yield of 20 wheat cultivars (16 bread wheat, Triticum aestivum; four durum wheat, Triticum durum cultivars) were investigated over 2 years under rainfed and irrigated conditions in Central Anatolia where drought and Zn deficiency cause substantial yield reductions. Plants were treated with (+Zn: 23 kg Zn ha−1, as ZnSO4·7H2O) and without (−Zn) Zn under rainfed and irrigated conditions. Both Zn deficiency and rainfed treatments resulted in substantial decreases in grain yield. Significant differences were determined between both bread wheat and durum wheat cultivars in terms of drought stress tolerance. Considering drought sensitivity indices over 2 years, the bread wheat cultivars Yayla‐305, Gerek‐79, Dagdas‐94 and Bolal‐2973 were found to be more drought‐tolerant than the other cultivars under both −Zn and +Zn treatments. Especially the durum wheat cultivars Cakmak 79 and Selcuklu 97 showed much greater drought susceptibility under Zn deficiency, and irrigation alone was not sufficient to obtain satisfying grain yield without Zn application. The results indicate that sensitivity to Zn deficiency stress became more pronounced when plants were drought‐stressed. The effect of irrigation on grain yield was maximized when Zn was adequately supplied, leading to the suggestion that efficient water use in Central Anatolia seems to be highly dependent on the Zn nutritional status of plants.

Effects of zinc deficiency on oral and periodontal diseases in rats

The aim of this study was to investigate the alterations of oral and periodontal tissues in zinc-deficient rats compared with control rats. The study was carried out on 14 Sprague-Dawley rats, cessation of lactation on the 24th day after birth. Rats were randomly divided into two groups. Group I rats were fed with a zinc-deficient diet and group II rats were fed with a zinc-containing diet. At the end of the fourth week on experimental diets, alterations of the oral tissues in both groups were recorded. In addition, the gingival index (GI-Löe-Silness), plaque index (PI-Silness-Löe) and periodontal pocket depth scores were recorded in order to assess periodontal tissue health in the rats. Then, blood samples were taken and the serum zinc levels measured by atomic absorption spectrophotometry. At the end of the experiment, oral tissue samples were investigated by light microscopy. Finally, the results of the two groups were compared by using the Student's t-test. The effects of zinc deficiency were observed at 10-16 d in rats. Although body weight, body length and tail length were retarded in zinc-deficient rats, they were advanced in rats fed with a zinc-containing diet. The mean plaque index and gingival index for group II rats were significantly lower than for group I rats (p<0.001), but there was no significant difference regarding pocket depth between the two groups of rats (p>0.05). Aphthous ulcer was often seen in the study group, where it was observed on the alveolar mucosa with a high rate of 29.9%. According to histological findings, there was no difference related to the epithelial keratinization of the hard palate between the two groups. However, hyperkeratosis was found on the dorsal surface of the tongue in zinc-deficient rats. The findings indicated that oral health was better in group II rats (those fed with a zinc-containing diet) than in group I (zinc-deficient) rats. Hyperkeratinization was more prominent in zinc-deficient rats. We suggest that zinc deficiency is a potential risk factor for oral and periodontal diseases.

Effects of zinc deficiency on rice growth and genetic factors contributing to tolerance.

Zinc (Zn) deficiency is the most widespread micronutrient disorder in rice (Oryza sativa), but efforts to develop cultivars with improved tolerance have been hampered by insufficient understanding of genetic factors contributing to tolerance. The objective of this paper was to examine alternative evaluation methods and to identify the most informative traits that would provide realistic information for rice breeders and to map quantitative trait loci (QTLs) associated with tolerance. Screening experiments in low-Zn nutrient solution and in a Zn-deficient field did not produce similar tolerance rankings in a set of segregating lines, which suggested that rhizosphere effects were of greater importance for lowland rice than internal Zn efficiency. The most severe symptom in the field was high plant mortality. The occurrence of leaf bronzing, usually regarded as indicative of susceptibility, did not necessarily concur with high plant mortality, which implied that both were under independent genetic control. The QTL mapping experiment conducted in the field with a population derived from a cross of IR74 (intolerant) with Jalmagna (tolerant) largely confirmed this. Four QTLs associated with plant mortality were detected, and only one of those colocalized with one of the four QTLs detected for leaf bronzing. The two most influential QTLs for plant mortality were detected on chromosomes 2 and 12. They explained 16.6% and 24.2% of the variation, and alleles of the tolerant donor parent Jalmagna reduced mortality by 16.6% and 14.8%, respectively. QTLs for plant mortality acted in a purely additive manner, whereas digenic epistatic interactions were important for leaf bronzing.

The role of intracellular zinc in chromium(VI)-induced oxidative stress, DNA damage and apoptosis

Several studies have demonstrated that zinc is required for the optimal functioning of the skin. Changes in intracellular zinc concentrations have been associated with both improved protection of skin cells against various noxious factors as well as with increased susceptibility to external stress. Still, little is known about the role of intracellular zinc in hexavalent chromium (Cr(VI))-induced skin injury. To address this question, the effects of zinc deficiency or supplementation on Cr(VI)-induced cytotoxicity, oxidative stress, DNA injury and cell death were investigated in human diploid dermal fibroblasts during 48 h. Zinc levels in fibroblasts were manipulated by pretreatment of cells with 100 μM ZnSO 4 and 4 or 25 μM zinc chelator TPEN. Cr(VI) (50, 10 and 1 μM) was found to produce time- and dose-dependent cytotoxicity resulting in oxidative stress, suppression of antioxidant systems and activation of p53-dependent apoptosis which is reported for the first time in this model in relation to environmental Cr(VI). Increased intracellular zinc partially attenuated Cr(VI)-induced cytotoxicity, oxidative stress and apoptosis by enhancing cellular antioxidant systems while inhibiting Cr(VI)-dependent apoptosis by preventing the activation of caspase-3. Decreased intracellular zinc enhanced cytotoxic effects of all the tested Cr(VI) concentrations, leading to rapid loss of cell membrane integrity and nuclear dispersion—hallmarks of necrosis. These new findings suggest that Cr(VI) as a model environmental toxin may damage in deeper regions residing skin fibroblasts whose susceptibility to such toxin depends among others on their intracellular Zn levels. Further investigation of the impact of Zn status on skin cells as well as any other cell populations exposed to Cr(VI) or other heavy metals is warranted.

Zinc deficiency and its inherited disorders -a review

Zinc is an essential trace element required by all living organisms because of its critical roles both as a structural component of proteins and as a cofactor in enzyme catalysis. The importance of zinc in human metabolism is illustrated by the effects of zinc deficiency, which include a diminished immune response, reduced healing and neurological disorders. Furthermore, nutritional zinc deficiency can be fatal in newborn or growing animals. While zinc deficiency is commonly caused by dietary factors, several inherited defects of zinc deficiency have been identified. Acrodermatitis enteropathica is the most commonly described inherited condition found in humans. In several of the few cases that have been reported, this disorder is associated with mutations in the hZIP4 gene, a member of the SLC39 family, whose members encode membranebound putative zinc transporters. Mutations in other members of this family or in different genes may account for other cases of acrodermatitis in which defects in hZIP4 have not been detected. Another inherited form of zinc deficiency occurs in the lethal milk mouse, where a mutation in ZnT4 gene, a member of the SLC30 family of transmembrane proteins results in impaired secretion of zinc into milk from the mammary gland. A similar disorder to the lethal milk mouse occurs in humans. In the few cases studied, no changes in ZnT4 orthologue, hZnT4, were detected. This, and the presence of several minor phenotypic differences between the zinc deficiency in humans and mice, suggests that the human condition is caused by defects in genes that are yet to be identified. Taking into account the fact that there are no definitive tests for zinc deficiency and that this disorder can go undiagnosed, plus the recent identification of multiple members of the SCL30 and SLC39, it is likely that mutations in other genes may underlie additional inherited disorders of zinc deficiency.

Impact of zinc deficiency on vibrio cholerae enterotoxin-stimulated water and electrolyte transport in animal model.

The effect of zinc deficiency on the function of the intestine to absorb water and electrolytes was studied in animal models, stimulated by Vibrio cholerae enterotoxin. Sprague-Dawley rats, used in the study, were divided into four groups: Zinc-deficient, ad libitum zinc-fed control, zinc weight-matched control, and zinc-deficient acutely-repleted. 14C-labelled polyethylene glycol solution was used for measuring the absorption capacity of the small intestine. Significantly lower absorption of water and sodium per cm of the intestine was observed in the zinc-deficient animals compared to the ad libitum zinc-fed control animals (p < 0.01). An improved absorption capacity was equally observed in the zinc-deficient acutely-repleted animals and ad libitum zinc-fed control group. The zinc-deficient animals showed four times greater cholera toxin-induced net secretions of water and sodium compared to the ad libitum zinc-fed group (p < 0.01), while a 40% reduction was observed in the zinc-deficient acutely-repleted group. The results suggest that zinc deficiency is associated with reduced absorption of water and electrolytes and increased secretion of the same stimulated by cholera toxin.