Expression Of Zinc Transporters Research Articles

Effect of the estrous cycle on zinc transporter expression in bovine cumulus-oocyte complexes and oviduct epithelial cells.

During the luteal and follicular phases of the estrous cycle, cumulus-oocyte complexes (COC) and oviduct epithelial cells (OEC) undergo notable physiological and morphological changes. Maintaining proper zinc (Zn) homeostasis is crucial in both somatic and germinal mammalian cells. This study aimed to assess the impact of the estrous phase (luteal or follicular) on Zn transporter expression in bovine COC and OEC (BOEC). The expression of Zn transporters Slc39a6 (ZIP6), Slc39a8 (ZIP8), Slc39a14 (ZIP14), Slc30a3 (ZnT3), Slc30a7 (ZnT7), and Slc30a9 (ZnT9) was analyzed in COC and BOEC from cows during the luteal or follicular phases. Gene expression of ZIP6, ZIP14, and ZnT9 was quantified in COC and BOEC. The gene expression in the remaining transporters could not be quantified due to low mRNA levels (ZIP8 and ZnT3 in COC and BOEC; ZnT7 in BOEC) or absence of expression (ZnT7 in COC). In COC, the relative expression (RE) of all three transporters was higher in the luteal phase compared to the follicular phase (P ≤ 0.05). In BOEC, the luteal phase increased the RE of ZIP 6 (P ≤ 0.05), decreased the RE of ZnT9 (P ≤ 0.05), and did not modify the RE of ZIP14 (P > 0.05) compared to the follicular phase. In conclusion, the study reveals differences in the gene expression of ZIP6, ZIP14, and ZnT9 according to the estrous cycle phase in ex vivo samples of bovine COC and OEC.

Zinc proteinate with moderate chelation strength enhances zinc absorption by upregulating the expression of zinc and amino acid transporters in primary cultured duodenal epithelial cells of broiler embryos.

Recent study showed that zinc (Zn) and amino acid transporters may be involved in enhancing Zn absorption from Zn proteinate with moderate chelation strength (Zn-Prot M) in the duodenum of broilers. However, the specific mechanisms by which Zn-Prot M promotes the above Zn absorption are unknown. Therefore, in this study, 3 experiments were conducted to investigate specific and direct effects of Zn-Prot M and Zn sulfate (ZnS) on Zn absorption and expression of related transporters in primary duodenal epithelial cells of broiler embryos so as to preliminarily address possible mechanisms. In experiment 1, cells were treated with 100 μmol Zn/L as ZnS or Zn-Prot M for 20, 40, 60, 80, 100, or 120min. Experiment 2 consisted of 3 sub-experiments. In experiment 2A, cells were treated with a Zn-unsupplemented basal medium (Control) or the basal medium supplemented with 100 or 200 μmol Zn/L as ZnS or Zn-Prot M for 60min; in experiment 2B, cells were treated with a Zn-unsupplemented basal medium (Control) or the basal medium supplemented with 200 μmol Zn/L of as the ZnS or Zn-Prot M for 120min; in experiment 2C, cells were treated with a Zn-unsupplemented basal medium (Control) or the basal medium supplemented with 400 or 800 μmol Zn/L as ZnS or Zn-Prot M for 120min. In experiment 3, cells were treated with a Zn-unsupplemented basal medium (Control) or the basal medium supplemented with 400 μmol Zn/L as ZnS or Zn-Prot M for 120min. The results of experiment 1 indicated that the minimum incubation time for saturable Zn absorption was determined to be 50.83min using the best fit line. The results in experiment 2 demonstrated that a Zn concentration of 400 μmol/L and an incubation time of 120min were suitable to increase the absorption of Zn from Zn-Prot M compared to ZnS. In experiment 3, Zn absorption across cell monolayers was significantly increased by Zn addition (P < 0.05), and was significantly greater with Zn-Prot M than with ZnS (P < 0.05). Compared to the control, Zn addition significantly decreased Zn transporter 10 and peptide-transporter 1 mRNA expression levels and increased y + L-type amino transporter 2 (y + LAT2) protein abundance (P < 0.05). Moreover, protein expression levels of zrt/irt-like protein 3 (ZIP3), zrt-irt-like protein 5 (ZIP5), and y + LAT2 were significantly greater for Zn-Prot M than for ZnS (P < 0.05). These findings suggest that Zn-Prot M promote Zn absorption by increasing ZIP3, ZIP5 and y + LAT2 protein expression levels in primary duodenal epithelial cells.

Placental Expression of Glucose and Zinc Transporters in Women with Gestational Diabetes

Background/Objectives: Gestational diabetes (GDM) is a metabolic disorder with altered glucose levels diagnosed in pregnant women. The pathogenesis of GDM is not fully known, but it is thought to be caused by impaired insulin production and insulin resistance induced by diabetogenic factors. The placenta may play an important role in the development of GDM. Glucose transporters (GLUTs) are responsible for the delivery of glucose into the foetal circulation. Placental zinc transporters regulate insulin and glucagon secretion, as well as gluconeogenesis and glycolysis. The aim of this study was to investigate the placental expression of GLUT3, GLUT4, GLUT7 and SLC30A8 in women with GDM. Furthermore, we evaluated whether the expression profiles of these transporters were correlated with clinical parameters. Methods: This study included 26 patients with GDM and 28 patients with normal glucose tolerance (NGT). Results: The placental expression of GLUT3 was significantly reduced in the GDM group, while the placental expression of GLUT4, GLUT7 and SLC30A8 was significantly upregulated in the GDM group. GLUT3 expression correlated significantly with body mass index (BMI) increase during pregnancy and body mass increase during pregnancy, while GLUT4 expression correlated negatively with BMI at birth. Conclusions: These results suggest the involvement of GLUT3 and GLUT4, GLUT7 and SLC30A8 in the pathogenesis of GDM.

Development of a live cell assay for the zinc transporter ZnT8

Zinc is an essential trace element that is involved in many biological processes and in cellular homeostasis. In pancreatic β-cells, zinc is crucial for the synthesis, processing, and secretion of insulin, which plays a key role in glucose homeostasis and which deficiency is the cause of diabetes. The accumulation of zinc in pancreatic cells is regulated by the solute carrier transporter SLC30A8 (or Zinc Transporter 8, ZnT8), which transports zinc from cytoplasm in intracellular vesicles. Allelic variants of SLC30A8 gene have been linked to diabetes. Given the physiological intracellular localization of SLC30A8 in pancreatic β-cells and the ubiquitous endogenous expression of other Zinc transporters in different cell lines that could be used as cellular model for SLC30A8 recombinant over-expression, it is challenging to develop a functional assay to measure SLC30A8 activity. To achieve this goal, we have firstly generated a HEK293 cell line stably overexpressing SLC30A8, where the over-expression favors the partial localization of SLC30A8 on the plasma membrane. Then, we used the combination of this cell model, commercial FluoZin-3 cell permeant zinc dye and live cell imaging approach to follow zinc flux across SLC30A8 over-expressed on plasma membrane, thus developing a novel functional imaging- based assay specific for SLC30A8. Our novel approach can be further explored and optimized, paving the way for future small molecule medium-throughput screening.

Zinc transporters expression profile in professional handball players supplemented with zinc

IntroductionZinc (Zn) deficiency has been described not only on general human health but also within the sports context –as negatively affecting performance–. Thus, Zn status assessment is of great interest for athletes, especially in order to correct deficiency states of this mineral. ObjectiveThe overall objective of this work was to assess Zn status in professional handball players during the competitive period (through plasma levels, dietary intake and gene expression of the Zn transporters), as well as to determine the effect of Zn supplementation. MethodsA total of twenty-two participants were recruited, –twelve belonged to the Control Group (CG) and ten male handball players comprised the experimental group (ATH-G)–, being monitored over a 2-month period with 2 evaluation moments: baseline (i.e., initial conditions) and follow-up (i.e., after 8 weeks of training and competition). Zn intake, plasma Zn levels, and gene expression of Zn transporters were obtained. ResultsPlasma Zn levels were higher in ATH-G than in CG at the end of Zn intervention (p ≤ 0.010). Moreover, differences in the gene expression profile of Zn transporters were observed in ATH-G –with the down-regulation of several Zn transporters–, compared to the CG at baseline (p ≤ 0.05). Likewise, differences in the Zn transporters expression were observed in ATH-G at 8 weeks (all, p ≤ 0.001) –with ZnT2, ZnT5, ZIP3, ZIP5, ZIP11, ZIP13 and ZIP14 transporters being up-regulated–. ConclusionHandball players seemed to have different nutritional needs for Zn, with differences in the gene expression of Zn transporters compared to controls. Zn intervention in our athletes may have influenced the expression of Zn transporters, indicating a potential increase in Zn transporters expression to mobilize Zn at the cellular level at 8 weeks of Zn intervention.

PIAS3 acts as a zinc sensor under zinc deficiency and plays an important role in myocardial ischemia/reperfusion injury

Alterations in zinc transporter expression in response to zinc loss protect cardiac cells from ischemia/reperfusion (I/R) injury. However, the underlying molecular mechanisms how cardiac cells sense zinc loss remains unclear. Here, we found that zinc deficiency induced ubiquitination and degradation of the protein inhibitor of activated STAT3 (PIAS3), which can alleviate myocardial I/R injury by activating STAT3 to promote the expression of ZIP family zinc transporter genes. The RING finger domain within PIAS3 is vital for PIAS3 degradation, as PIAS3-dRing (missing the RING domain) and PIAS3-Mut (zinc-binding site mutation) were resistant to degradation in the setting of zinc deficiency. Meanwhile, the RING finger domain within PIAS3 is critical for the inhibition of STAT3 activation. Moreover, PIAS3 knockdown increased cardiac Zn2+ levels and reduced myocardial infarction in mouse hearts subjected to I/R, whereas wild-type PIAS3 overexpression, but not PIAS3-Mut, reduced cardiac Zn2+ levels, and exacerbated myocardial infarction. These findings elucidate a unique mechanism of zinc sensing, showing that fast degradation of the zinc-binding regulatory protein PIAS3 during zinc deficiency can correct zinc dyshomeostasis and alleviate reperfusion injury.

Effect of estrogen and progesterone on intracellular free zinc and zinc transporter expression in bovine oviduct epithelial cells

Zinc (Zn) plays essential roles in numerous cellular processes. However, there is limited understanding of Zn homeostasis within the bovine reproductive system. This study investigated the influence of estradiol (E2) and progesterone (P4) on Zn transporter expression and intracellular free Zn levels in bovine oviduct epithelial cells (BOEC). For this purpose, cells were harvested from slaughtered cows and cultured in vitro. Intracellular Zn concentrations were measured using FluoZin-3AM staining, while real-time polymerase chain reaction assessed Zn transporter gene expression and quantification. Overall, our results confirmed the gene expression of all the evaluated Zn transporters (ZIP6, ZIP8, ZIP14, ZnT3, ZnT7 and ZnT9), denoted and the active role of E2 and P4 in intracellular Zn regulation. Our findings suggest an interaction between Zn, E2 and P4.

A Short-Term Zinc-Deficient Diet Maintains Serum Calcium Concentrations through Ca Absorption-Related Gene Expression in Rats.

We investigated the effects of short-term dietary zinc deficiency on zinc and calcium metabolism. Four-week-old male Wistar rats were divided into two pair-fed groups for a 1-wk treatment: zinc-deficient group (ZD, 1 ppm); control group (PF, 30 ppm). The mRNA expression of zinc transporters, such as Slc39a (Zip) 4, Zip5, Zip10, and Slc30a (ZnT) 1, in various tissues (liver, kidney, and duodenum) quickly responded to dietary zinc deficiency. Although there was no significant difference in serum calcium concentrations between the PF and ZD groups, serum 1,25-dihydroxycholecalciferol (1,25(OH)2D3) was higher in the ZD group than in the PF group. Moreover, short-term zinc deficiency significantly increased mRNA expression of transient receptor potential (TRP) cation channel subfamily vanilloid (V) member 6, S100 calcium binding protein G (S100g), and ATPase plasma membrane Ca2+ transporting 1 (Atp2b1) in the duodenum. Furthermore, short-term zinc deficiency increased vitamin D receptor (VDR) and cytochrome P450 family 24 subfamily A member 1 (Cyp24a1) mRNA expression in the kidney. These findings suggested that short-term zinc deficiency maintains serum calcium concentrations through Ca absorption-related gene expression in the duodenum, and that short-term zinc deficiency induced the expression of Cyp24a1 in kidney in response to an increase in the serum 1,25(OH)2D3 level.

Reduced expression of bZIP19 and bZIP23 increases zinc and cadmium accumulation in Arabidopsis halleri.

Zinc is an essential micronutrient for all living organisms. When challenged by zinc-limiting conditions, Arabidopsis thaliana plants use a strategy centered on two transcription factors, bZIP19 and bZIP23, to enhance the expression of several zinc transporters to improve their zinc uptake capacity. In the zinc and cadmium hyperaccumulator plant Arabidopsis halleri, highly efficient root-to-shoot zinc translocation results in constitutive local zinc deficiency in roots and in constitutive high expression of zinc deficiency-responsive ZIP genes, supposedly boosting zinc uptake and accumulation. Here, to disrupt this process and to analyze the functions of AhbZIP19, AhbZIP23 and their target genes in hyperaccumulation, the genes encoding both transcriptional factors were knocked down using artificial microRNAs (amiRNA). Although AhbZIP19, AhbZIP23, and their ZIP target genes were downregulated, amiRNA lines surprisingly accumulated more zinc and cadmium compared to control lines in both roots and shoot driving to shoot toxicity symptoms. These observations suggested the existence of a substitute metal uptake machinery in A. halleri to maintain hyperaccumulation. We propose that the iron uptake transporter AhIRT1 participates in this alternative pathway in A. halleri.

Transgenerational Effects of Maternal Zinc Deficiency on Zinc Transporters in Drosophila melanogaster.

Maternal nutrition, including the availability of micronutrients such as zinc, influences the health of the offspring. Using Drosophila melanogaster, we studied the impact of zinc deficiency on development and reproduction, as well as the effects of maternal zinc status on the offspring's expression of zinc transporters across F1 to F3 generations. Zinc deficiency was induced by adding N,N,N',N'-Tetrakis (2-pyridylmethyl)-ethylenediamine (TPEN) to the diet on which the eggs representing the F0 generation flies were laid. Then, virgin F0 females were mated with control males to produce F1, and subsequently thereafter to generate F2 and F3. Offspring from F1 to F3 were analyzed for body zinc status and zinc transporter mRNA levels. We found that zinc deficiency significantly (p < 0.05) impaired the development of flies, as evidenced by a reduced eclosion rate of zinc-deficient flies. Similarly, zinc deficiency significantly (p < 0.05) reduced the egg-laying rate in F0 flies, highlighting its impact on reproductive functions. Also, zinc levels were consistently lower in the F0 and persisted in subsequent generations for both male and female offspring, indicating transgenerational alterations in zinc status. Furthermore, gene expression analysis revealed significant (p < 0.05) variations in the mRNA levels of dZip42C.1, dZnT63C, dZip71B, and dZnT35C genes across different generations and between male and female offspring. These findings indicate gender-specific dynamics of gene expression in response to zinc deficiency, suggesting potential regulatory mechanisms involved in maintaining zinc homeostasis. Our study emphasizes the detrimental effects of zinc deficiency on development and reproduction in Drosophila and highlights potential implications for offspring and human health.

Hyperuricemia Induces Reproductive Damage in Male Rats through Zinc Homeostasis Imbalance and Oxidative Stress

Studies have reported the adverse effects of hyperuricemia on male reproduction, but the mechanism is still unclear. The purpose of this study is to explore the mechanism of hyperuricemia on reproductive system damage in male rats. The rats were divided into a control group and a model group. Rats were given hypoxanthine and potassium oxonate dissolved in 0.5% (w/v) sodium carboxymethyl cellulose solution to induce the hyperuricemia (HUA) model. After 6 weeks, the blood, testis, and epididymis tissues of the anesthetized rats were collected for further experiments and analysis. Compared with the control rats, the serum uric acid of HUA rats was significantly increased, and the serum testosterone, sperm count, and motility were significantly decreased. The protein expression of testosterone-related molecules CYP11A1, 3β-HSD, and StAR was downregulated in the testis of HUA rats. The protein expression of blood–testis barrier (BTB) related molecules ZO-1 and Connexin43 was downregulated in the testis of HUA rats. Compared with the control group, the zinc content and zinc-containing enzymes (ALP and LDH) were decreased, and the mRNA and protein expression of zinc transporters (ZnT4 and ZIP7) were downregulated in the testis of HUA rats. Furthermore, the level of MDA increased and the activities of CAT, GSH-PX, and SOD decreased in the testicular tissue of HUA rats. The PI3K/AKT/mTOR pathway in the testis of HUA rats was activated. However, there was no significant change in the protein expression of autophagy associated molecules LC3, Beclin1, and ATG5 in the testis of HUA rats. Thus, the conclusion is that hyperuricemia can lead to the destruction of BTB, impaired testosterone synthesis, and decreased sperm count and motility in male rats, mainly by inducing zinc homeostasis imbalance and oxidative stress, rather than autophagy.

Upregulation of Intracellular Zinc Ion Level after Differentiation of the Neural Stem/Progenitor Cells In Vitro with the Changes in Gene Expression of Zinc Transporters.

We measured the intracellular zinc ion concentration of murine fetal neural stem/progenitor cells (NSPCs) and that in the differentiated cells. The NSPCs cultured with 1.5μM Zn2+ proliferated slightly faster than that in the zinc-deficient medium and the intracellular zinc concentration of the NSPCs and that of their differentiated cells (DCs) cultured with 1.5μM Zn2+ was 1.34-fold and 2.00-fold higher than those in the zinc-deficient medium, respectively. The zinc transporter genes upregulated over the 3.5-fold change were Zip1, Zip4, Zip12, Zip13, ZnT1, ZnT8, and ZnT10 whereas the only downregulated one was Zip8 during the differentiation of NSPCs to DCs. The cell morphologies of both NSPCs and DCs in the low oxygen culture condition consisting of 2%O2 and 5%CO2, the high carbon dioxide condition consisting of 21%O2 and 10%CO2, and the normal condition consisting of 21%O2 and 5%CO2 were essentially the same each other. The expression of Zip4, Zip8, Zip12, and Zip14 was not drastically changed depending on the O2 and CO2 concentrations.

226 Modulation of Zinc, Copper and Iron Transporters in Weaned Pigs Fed Different Dietary Zinc/Copper Ratios

Abstract This study evaluated the impact of different dietary zinc/copper ratios on the gene expression of zinc (Zn), copper (Cu), and iron (Fe) transporters in jejunum and liver of weaned pigs. Piglets (n = 160) were weaned at 21 days of age (d 21; 7.81 ± 0.25 kg) and fed a basal post-weaning diet (without antibiotics) supplemented (n = 40/treatment) with 100 (LZn) or 3,000 (HZn) mg/kg of Zn as ZnO in combination with 6 (LCu) or 130 (HCu) mg/kg of Cu as CuSO4 until d 42. Piglets were sacrificed at d 21, d 28, d 35, and d 42 (n = 10 animals∙treatment -1∙day-1) for harvesting jejunum and liver samples. The mRNA expression of Zn, Cu, and Fe transporters was evaluated by quantitative real-time PCR. Data were analyzed using a 2x2x3 factorial design (two Zn levels, two Cu levels, and three slaughter days) and results are presented as fold-change relative to pre-treatment values (d 21). For Zn-related genes, jejunum Zip4 expression was least for HZn from d 28 (Zn effect; P ≤ 0.01; Table 1) and Zip5 was greatest for HZn at d 28 (Zn effect; P = 0.04). On d 42, the greatest values for jejunal Zip4 were observed with LZnHCu (interaction Zn x Cu x time; P = 0.05). For Znt1 in jejunum and liver, mRNA expression was greatest for HZn from d 28 (Zn effect; P ≤ 0.01) whereas Zip5 was greatest in liver for HZn at d 28 and d 35 (Zn effect; P ≤ 0.04). On d 35, the least values for hepatic Zip5 were observed with LZnHCu (interaction Zn x Cu x time; P = 0.04). For Cu-related genes, no treatment effect (P ≥ 0.12) was detected for Crt1 and Atox1 in jejunum and liver. In both tissues, Mt3 expression was greatest for HZn from d 28 (Zn effect; P ≤ 0.01). No treatment effect was detected (P = 0.53) for Atp7a expression in jejunum. However, for Atp7b in liver, values were greatest for HZn from d 35 (Zn effect; P ≤ 0.01). For Fe-related genes, no treatment effect (P ≥ 0.18) was detected for Heph, Tfrc and Fpn1 in jejunum and for Dmt1, Tfrc and Hamp in liver. In jejunum, Dmt1 was greatest for LZn at d 28 and d 42 (Zn effect; P ≤ 0.01) whereas Fth1 was greatest in HZn groups from d28 (Zn effect; P ≤ 0.01) and for HCu at d42 (Cu effect; P = 0.04). In liver, Fth1 and Fpn1 were greatest for HZn from d28 (Zn effect; P ≤ 0.02). In conclusion, among the present different dietary zinc/copper ratios, most treatment effects on intestinal and hepatic Zn, Cu and Fe transporters originated from dietary ZnO levels suggesting a major contribution of Zn in modulating the metabolism of these trace minerals in post-weaning piglets.

Zinc Transporters in the Livers of Healthy Male Wistar Rats: An Investigation of the Effects of Aerobic Exercise and Supplementation with Pumpkin Seed and White Pea

Background: The current study aims to investigate the impacts of aerobic exercise with pumpkin seed oil and white pea extract supplementation on the gene expression of the liver zinc transporters of healthy male Wistar rats. Methods: In this experimental study, 60 male Wistar rats (130 - 150 g, aged 4-6 weeks old) were divided into 6 groups (n = 10/groups) by randomization. These groups include (1) saline control, (2) saline training, (3) pumpkin seed oil control, (4) pumpkin seed oil training, (5) control-pea, and (6) training-pea. The aerobic exercise protocol consisted of running at a velocity of 25 m/min, 5 days a week and for 6 weeks. Supplement groups received 4 ml/kg/day of pumpkin seed oil and 2 g/kg/day of white pea extract through oral gavage. Gene expression levels of ZnT5, ZnT9, and ZIP14 of liver tissue were determined through real-time PCR, and serum levels of Zn were measured using the ICP-EOS technique approximately 48 hours after the final session of the training program. Data were analyzed by one-way ANOVA and Tukey post-hoc tests (P &lt; 0.05). Results: Regarding the results of one-way ANOVA, there were no significant changes in serum Zn levels (P = 0.418) as well as gene expression levels of ZnT5 and ZIP14 among intervention groups (P = 0.586 and 0.677, respectively), but ZnT9 gene expression level was significantly changed among the study groups (P = 0.029). Also, the results of the Tukey test showed that six weeks of aerobic exercise along with pumpkin seed oil supplementation had the greatest effect on ZnT5 gene expression. Conclusions: Findings showed that aerobic training along with pumpkin seed oil supplementation had the greatest impact on the up-regulation of ZnT5 as a Zn transporter to retain the blood Zn levels in healthy trained rats, suggesting that pumpkin seed oil can be an effective ergogenic aid for improving circulatory Zn levels.

Zinc supplementation alters tissue distribution of arsenic in Mus musculus

Arsenic occurs naturally in the environment and humans can be exposed through food, drinking water and inhalation of air-borne particles. Arsenic exposure is associated with cardiovascular, pulmonary, renal, immunologic, and developmental toxicities as well as carcinogenesis. Arsenic displays dose-depen toxicities in target organs or tissues with elevated levels of arsenic. Zinc is an essential micronutrient with proposed protective benefits due to its antioxidant properties, integration into zinc-containing proteins and zinc-related immune signaling. In this study, we tested levels of arsenic and zinc in plasma, kidney, liver, and spleen as model tissues after chronic (42-day) treatment with either arsenite, zinc, or in combination. Arsenite exposure had minimal impact on tissue zinc levels with the exception of the kidney. Conversely, zinc supplementation of arsenite-exposed mice reduced the amount of arsenic detected in all tissues tested. Expression of transporters associated with zinc or arsenic influx and efflux were evaluated under each treatment condition. Significant effects of arsenite exposure on zinc transporter expression displayed tissue selectivity for liver and kidney, and was restricted to Zip10 and Zip14, respectively. Arsenite also interacted with zinc co-exposure for Zip10 expression in liver tissue. Pairwise comparisons show neither arsenite nor zinc supplementation alone significantly altered expression of transporters utilized by arsenic. However, significant interactions between arsenite and zinc were evident for Aqp7 and Mrp1 in a tissue selective manner. These findings illustrate interactions between arsenite and zinc leading to changes in tissue metal level and suggest a potential mechanism by which zinc may offer protection from arsenic toxicities.

Galvanized material is a promising approach to control Amyloodinium ocellatum infection in fishes

Amyloodinium ocellatum is a worldwide distributed dinoflagellate that infects marine and brackish water fish, causing mass mortality and economic loss. This study evaluated the efficacy of the seawater immersed with galvanized materials (IGM seawater) in controlling A. ocellatum reinfection in susceptible host Trachinotus ovatus. Furthermore, the toxicity of IGM seawater to the dinospores infectivity, tomonts development, and trophonts parasitism was determined in Acanthopagrus latus. The expression of zinc transporters in A. latus gills and livers was also detected after A. latus exposure to IGM seawater. The results revealed that parasite abundances on infected T. ovatus were significantly decreased in the seawater immersed with 0.1 m2/m3 of galvanized iron mesh for 2 days ([0.1–2 d] group) or galvanized iron plates with a 56.25% tank coverage for 1 day ([56.25% - 1 d] group). Besides, the survival rates of the infected T. ovatus in the [0.1–2 d] and [56.25% - 1 d] group were 100% on the 14th-day post-infection, while 0% in the control group. The infectivity of dinospores was significantly inhibited in the seawater immersed with 0.4 m2/m3 of galvanized iron mesh for 2 days ([0.4–2 d] group) by 89.50%. In addition, the reduction of trophonts in the [0.4–2 d] group was 46.24% compared to the control group. However, the hatching rate of tomonts in the seawater immersed with 0.4 m2/m3 of galvanized iron mesh for either 1, 2, or 3 days was 100% at 48th hr post-treatment. At the same time, the zinc ion concentrations in the IGM seawater group were continuously increased. On the contrary, the mRNA levels of zinc transporters ZIP7 and ZIP11 in the liver of A. latus exposure to IGM seawater were significantly down-regulated. Therefore, A. latus acclimatizes to a high‑zinc environment by reducing zinc ions influx to maintain intracellular zinc homeostasis. These results imply that using galvanized material is a promising approach to controlling A. ocellatum infection in fish.

Zinc supplementation and ractopamine hydrochloride impact gene expression of zinc transporters in finishing beef steers

Zinc is a trace mineral of interest for optimizing growth in feedlot cattle due to its roles in many physiological functions, including growth. Twenty-four Angus-cross steers (467 ± 13 kg) were used to assess the effects of supplemental Zn and ractopamine hydrochloride (RAC) on trace mineral concentrations and muscle gene expression. Four GrowSafe-equipped pens were randomly assigned to treatments (1 pen of six steers/treatment): 0 (CON), 60 (LOW), 120 (MED) or 180 (HI) mg supplemental Zn/kg DM (Availa-Zn, Zinpro). Dietary Zn treatments were initiated on d 0 and RAC supplementation (300 mg·steer·-1·d-1; Actogain45, Zoetis) began on d 53. Blood, liver and muscle (longissimus thoracis) samples were collected from all steers on d -4, 48, and 67. The LOW treatment was removed from gene expression analyses due to &amp;lt; 3 steers being represented for 14 of 22 genes. Data were analyzed using ProcMixed of SAS with the fixed effect of treatment and steer as the experimental unit; orthogonal linear and quadratic contrast statements were used to compare treatments. On d 48 and 67, there were linear and quadratic trends for plasma Zn to be greater in Zn-supplemented steers than CON (P ≤ 0.10). On d 48, there was a tendency for a quadratic decrease on the expression of SLC30A4 (P ≤ 0.07) but no other differences due to treatment. On d 67, several genes involved in Zn transport and storage (MTA1, SLC39A7, SLC39A8, SLC39A9, SLC39A10, SLC39A13) were decreased (P ≤ 0.08), suggesting increased growth influences intracellular Zn trafficking and demands.

Effects of Zinc Status on Expression of Zinc Transporters, Redox-Related Enzymes and Insulin-like Growth Factor in Asian Sea Bass Cells.

Since Asian sea bass is one of the economically most important fish, aquaculture conditions are constantly optimized. Evidence from feeding studies combined with the current understanding of the importance of zinc for growth and immune defense suggest that zinc supplementation may be a possible approach to optimize aquacultures of Asian sea bass. To investigate the effects of zinc deficiency and zinc supplementation, cells from Asian sea bass were incubated in culture medium with different zinc contents. The expression of genes, important for zinc homeostasis, redox metabolism, and growth hormones was analyzed using RT-PCR. Zinc deficiency induced the expression of certain zinc transporters (ZIP14, ZIP10, ZIP6, ZIP4, ZnT4, ZnT9) as well as of SOD1, IGF I and IGF II, while expression of ZnT1 and metallothionein (MT) was reduced. Zinc supplementation decreased the expression of ZIP10, while expression of ZnT1 and MT were elevated. No differences in the effects of zinc supplementation with zinc sulfate compared to supplementation with zinc amino acid complexes were observed. Thus, extracellular zinc conditions may govern the cellular zinc homeostasis, the redox metabolism and growth hormone expression in cells from Asian sea bass as reported for other fish species. Our data indicate that supplementing aquacultures with zinc may be recommended to avoid detriments of zinc deficiency.

“Block and attack” strategy for tumor therapy through ZnO2/siRNA/NIR‐mediating Zn2+‐overload and amplified oxidative stress

AbstractIntracellular zinc ion (Zn2+) accumulation disrupts the Zn2+ homeostasis, providing an ion‐overloading anticancer strategy with great potential. The self‐adaptation of tumor cells to ion concentration, however, puts forward higher requirements for the design of ion‐overloading strategy. Herein, “block and attack” antitumor strategy was applied through a composite nanomaterials (UHSsPZH NPs). The strategy demonstrated powerful ion interference ability through both “blocking” the efflux of excess Zn2+ via gene silencing and “attacking” tumor cells via target delivery of ZnO2. After cellular internalization, ZnO2 was degraded to Zn2+ and hydrogen peroxide (H2O2), and the gene expression of zinc transporter 1 (ZnT1) was silenced by targeting of released siRNA, which together caused intracellular Zn2+‐overload. Disorder of Zn2+ further interfered with intracellular Ca2+ homeostasis, inhibited the electron transport chain and promoted the production of endogenous reactive oxygen species (ROS), which assisted the “attack” to tumor cells together with the exogenous ROS generated by UHSsPZH NPs under 980 nm laser irradiation. In summary, this work supplies a “block and attack” strategy for the application of ion homeostasis interference in tumor therapy.

Differences in Nutrient Uptake Can Influence the Performance of Citrus Rootstocks under Huanglongbing Conditions

Huanglongbing {HLB [Candidatus Liberibacter asiaticus (C Las)]} has been one of the biggest challenges in citrus (Citrus sp.) production in Florida and wherever it is present. HLB-affected trees show significant shoot and root dieback, fruit drop, and reduction in yield. Currently, there is no cure for HLB, and there is no commercial HLB-resistant germplasm. Nonetheless, intensive nutrient management has been promising for citrus growers. The nutrient requirement of HLB-affected trees seems to be greater than that of healthy citrus trees. By understanding the nutrient uptake potential of rootstocks, fertilizer programs can be customized accordingly to enhance the performance of a rootstock in existing groves. Moreover, a reduction in the application of nutrients is possible by planting rootstocks with a high nutrient absorption capacity. Use of rootstocks with good nutrient uptake efficiency can take some burden off the growers who are intensively managing HLB-affected citrus groves. Therefore, the objective of this study was to evaluate and understand the nutrient uptake potential of the citrus rootstocks. To achieve this objective, a 100% hydroponic greenhouse study was conducted with six rootstocks with a range of tolerance to HLB. Several physiological and molecular tools were applied to evaluate the rootstocks for their nutrient uptake potential. A+Volk × O-19 (HLB-tolerant) rootstock had greater nutrient uptake efficiency, whereas US-896 (HLB-susceptible) had lesser nutrient uptake efficiency. Swingle, one of the most popular pre-HLB rootstocks, had poor zinc uptake and the least expression of ZINC TRANSPORTER, suggesting that zinc applications should be emphasized in Swingle plantings. US-896 rootstock expressed the least level of nutrient transporter genes, such as IRON TRANSPORTER. UFR-4 (a good performer under HLB conditions) had a large root biomass, but the uptake efficiency for nutrients was poor, suggesting that the nutrient uptake potential is a complex process that is not solely dependent on root biomass. This study is unique because it is one of the first citrus studies to report nutrient uptake efficiency and the potential of rootstocks. The information presented can be used to improve performance or select better-performing rootstocks under HLB conditions.