Expression data from xenograft HuH7 mice treated with Zinc Acexamate and HuH7 cell line
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE277019 | GEO | 2025/01/01
REPOSITORIES: GEO
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Project description:Expression data from xenograft HuH7 mice treated with Zinc Acexamate and HuH7 cell line
| PRJNA1160232 | ENA
Project description:Objective: To determine the oxidative stress during cycles of chemotherapy in patients after surgery for colorectal cancer, with or without oral zinc supplementation. Subjects: Twenty four adults from both genders participated in this study. All patients underwent stage II, III or IV colorectal cancer surgical resection and were starting chemotherapy in HCFMRP- USP. Patients were randomized into two groups. The first one (QTx-Zn Group, n=10) received 70 mg/d of zinc orally and the second one received placebo (QTx-Placebo Group, n=14) for 16 weeks. The study also included 30 healthy volunteers matched for age, gender and socioeconomic status, who received 70 mg/d of zinc supplement (Control-Zn Group, n=21) or placebo (Control-Placebo Group, n=9) for 16 weeks. Methods: The questionnaires about dietary intake (semiquantitative food frequency and food record), fatigue and quality of life (FACIT-F) and questionnaires that assess the side effects of chemotherapy (CTCAE) were evaluated. Anthropometry and bioelectrical impedance measurements were made. Blood collection was performed before the 1st, 2nd, 3rd and 4th cycles of chemotherapy (median duration of 21 days among cicles). Routine laboratory tests, vitamin E and markers anti and pro-oxidants (MDA, SOD, GPx and isoprostane) ere determined. The control group underwent the same procedures, except for chemotherapy. A longitudinal linear mixed effects model was adjusted for each of the variables of interest. The models were fitted using PROC MIXED of SAS version 9 (SAS, CARY, NC, USA). To analyze the association of categorical variables in the different items of the CTCAE, the investigators used the Fisher exact test. Results: The oral zinc supplementation was sufficient to increase plasma levels of zinc and did not alter food intake, body composition and routine laboratory evaluation of patients undergoing chemotherapy for colorectal cancer. Compared with QTx-Placebo Group, QTx-Zn Group showed lower prevalence of complaint on the salivary gland (17 vs. 75%). Fatigue (43 ± 6 vs. 36 ± 13) and quality of life (126 ± 160 vs. 116 ± 27) has become worst in the period between the 1st and 4th cycles of QTx in QTx-Placebo Group. When compared with QTx-Placebo Group, QTx-Zn Group had higher values of SOD before the 1st (2297 ± 503 vs. 1604 ± 352 USOD/g Hb), 2nd (2037 ± 515 vs. 1712 ± 417 USOD/g Hb) and 4th (2202 ± 323 vs. 1821 ± 360 USOD/g Hb) cycles of QTx. GPx values decreased in QTx-Zn Group before the 3rd cycle of QTx (48.5 ± 7.0 vs. 54.3 ± 2.3 mol NADPH/min/gHb). Conclusions: These data suggest that zinc supplementation reduces complaints related to the change in salivary gland, preserving the quality of life and preventing the worsening of fatigue. The increase in SOD can be attributed to zinc supplementation per se, whereas this mineral is a cofactor that endogenous antioxidant enzyme. The highest activity of SOD increases the production of H2O2, whose detoxification involves the participation of GPx, justifying its reduction. There were no changes in plasma levels of vitamin E, MDA and isoprostane during the study period. Considering the values of MDA and isoprostane, the data indicate that regardless of zinc supplementation, the lipid peroxidation of the cell membrane was unchanged during chemotherapy.
| 2164178 | ecrin-mdr-crc
Project description:In the present study, we studied the effect of dietray zinc (Zn) supplementation on the transcriptome profile of lactating ewes. The main objective was to evaluate the effect of Zn-supplementation on the overall transcriptome and the altered pathways and biological processes in lactating ewes. A previously custom-designed oligo microarray platform (GPL20576) was used to profile the transcriptome of 15 ewes at two time points [T0 (before supplementation) and T40 (after 40-days supplementation period; n = 30). The Isolated and purified total RNAs were individually hybridized to the custom (4x44k) DNA microarray. The comparison of control and treated animal transcriptomes revealed a large set of differentially expressed genes. Functional analysis showed several pathways and biological processes that have been altered following Zn-supplementation to the diet.
2017-10-22 | GSE74779 | GEO
Project description:Zinc (Zn) is an essential trace element for all life forms. Zn supplementation has been used to treat diarrheal disease in children, and in the U.S. swine industry at pharmacological levels to promote growth and fecal consistency, but underlying mechanisms explaining these beneficial effects remain unknown. Thus, we hypothesized that the benefits of pharmacological Zn supplementation were a result of changes in gene expression. For this study, liver RNA from newly weaned pigs fed dietary Zn as Zn oxide for 14 days at either adequate (150 Zn/kg) or pharmacological (2000 mg Zn/kg) levels was evaluated using a 70-mer oligonucleotide microarray. Interrogation of this microarray revealed 658 annotated transcripts (FDR ≤ 0.05) affected by pharmacological Zn supplementation. Relative real-time RT-PCR was used to confirm differential expression of two genes. Results suggest that feeding pharmacological Zn (2000 mg Zn/kg) affects genes involved in reducing oxidative stress and in amino acid metabolism, which are essential for cell detoxification and proper cell function.
2008-10-02 | GSE11972 | GEO
Project description:Zinc (Zn) is an essential trace element for all life forms. Zn supplementation has been used to treat diarrheal disease in children, and in the U.S. swine industry at pharmacological levels to promote growth and fecal consistency, but underlying mechanisms explaining these beneficial effects remain unknown. Thus, we hypothesized that the benefits of pharmacological Zn supplementation were a result of changes in gene expression. For this study, liver RNA from newly weaned pigs fed dietary Zn as Zn oxide for 14 days at either adequate (150 Zn/kg) or pharmacological (2000 mg Zn/kg) levels was evaluated using a 70-mer oligonucleotide microarray. Interrogation of this microarray revealed 658 annotated transcripts (FDR ≤ 0.05) affected by pharmacological Zn supplementation. Relative real-time RT-PCR was used to confirm differential expression of two genes. Results suggest that feeding pharmacological Zn (2000 mg Zn/kg) affects genes involved in reducing oxidative stress and in amino acid metabolism, which are essential for cell detoxification and proper cell function. Oligonucleotide microarrays used for this study consisted of 13,297 70-mer oligos (Pig Array-Ready Oligo Set v. 1.0 and Pig Oligo Extension Set v. 1.0, Qiagen, Inc., Valencia, CA) each spotted once on a single slide. Slides were printed at the Michigan State University Research Technology Support Facility. Oligonucleotides spotted in multiple locations for use as potential controls included 76 Arabidopsis thaliana gene spots, 17 beta tubulin spots, 17 glyceraldehyde-3-phosphate dehydrogenase spots, 85 heat shock protein gene spots, 69 ribosomal protein gene spots, 112 randomly generated negative control spots and 470 blanks. The microarray was screened with the Zn150 and Zn2000 samples, and four microarray slides were screened. Zn150 samples were randomly paired with Zn2000 samples. Two samples from each treatment were labeled with Cy3 and the other two were labeled with Cy5.
2008-10-02 | E-GEOD-11972 | biostudies-arrayexpress
Project description:Zinc is an essential nutrient because of its role in catalysis and in stabilizing protein structure, but excess zinc can also be deleterious. Four nutritional zinc states have been identified in the alga Chlamydomonas reinhardtii: zinc toxic, zinc replete, zinc deficient and zinc limited. Growth is inhibited in zinc-limited and zinc toxic cells relative to zinc-replete cells, while zinc-deficiency is visually asymptomatic but distinguished by the accumulation of transcripts encoding ZIP family transporters. To identify targets of zinc deficiency and mechanisms of zinc acclimation, we used RNA-seq to probe zinc nutrition responsive changes in gene expression. We identified a subset of genes encoding zinc-handling components, including ZIP family transporters and candidate zinc chaperones. In addition, we noted an impact on two other regulatory pathways, the carbon concentrating mechanism (CCM) and the nutritional copper regulon. Targets of transcription factor Ccm1 and various CAH genes are up-regulated in zinc-deficiency, as a likely consequence of reduced carbonic anhydrase activity, which is validated by mass spectrometry and immunoblot analysis of Cah1, Cah3 and Cah4. Chlamydomonas is therefore not able to grow photoautotrophically in air in zinc limiting conditions, but supplementation with 1% CO2 restores growth to wild-type rates, suggesting that the inability to maintain CCM is a major consequence of zinc limitation. Surprisingly, we noted also that the Crr1 regulon, which responds to Cu limitation, is also turned on in zinc deficiency, and in fact, Crr1 is required for growth in zinc-limiting conditions. Zinc deficient cells are functionally copper deficient, as evidenced by reduced plastocyanin abundance, even though they hyperaccumulate copper up to 50-fold over normal levels. We suggest that zinc-deficient cells sequester Cu in a bio-unavailable form, perhaps to prevent mis-metallation of critical zinc sites. Zn-limited wild-type cells were generated by transfer of cells from the first round of growth in medium with no supplemental Zn into TAP medium supplemented or not with 2.5 µM Zn-EDTA The control samples for this study are represented in GSE25622
2013-05-03 | E-GEOD-41096 | biostudies-arrayexpress
Project description:ICP-MS analysis of Streptococcus pneumoniae D39 reveals a high cell-associated manganese (Mn(II)) concentration that is comparable to that of zinc (Zn(II)). Stressing these cells with 100-200 µM Zn(II) leads to a slow-growth phenotype and a reduction in total Mn(II) concentration, with no decrease in the concentrations of other metal ions. Supplementation of the growth media with as little as 10 µM Mn(II) fully restores wildtype growth patterns and normal levels of cell-associated Mn(II). DNA microarray analysis reveals that zinc stress induces the expected upregulation of czcD (encoding a zinc effluxer), but also a pleiotropic transcriptional response suggestive of mild cell wall stress. Genes encoding a nitric oxide detoxification system (nmlR) and the Mn(II) uptake system (psaABC) are also induced. We conclude that Zn(II) toxicity results in a cytoplasmic Mn(II) deficiency, possibly caused by competition at the Mn(II) uptake transporter protein PsaA.
2011-02-02 | GSE23504 | GEO
Project description:Elucidation of molecular basis of Iron and zinc homeostasis is crucial to breed iron and zinc use efficient and iron -zinc biofortified maize cultivars. The present investigation was framed to decipher the global expression snapshot maize seedlings in response to iron and zinc starvtion. Genome-wide transcriptome assay was performed with ~18,000 transcripts distributed across the maize genome, in maize seedlings after exposing the seedlings to three Fe and Zn stress treatments (+Fe–Zn, –Fe+Zn, –Fe–Zn) along with control (+Fe+Zn). Microarrays were used to study the global gene expression pattern iron and zinc starvation responsive genes in maize.
2021-01-04 | GSE122581 | GEO
Project description:Zinc (Zn) deficiency is a prevalent micronutrient insufficiency. Although the gut is a vital organ for Zn utilization, and Zn deficiency is associated with impaired intestinal permeability and a global decrease in gastrointestinal health, alterations in the gut microbial ecology of the host under conditions of Zn deficiency have yet to be studied. Using the broiler chicken (Gallus gallus) model, the aim of this study was to characterize distinct cecal microbiota shifts induced by chronic dietary Zn depletion. We demonstrate that Zn deficiency induces significant taxonomic alterations and decreases overall species richness and diversity, establishing a microbial profile resembling that of various other pathological states. Through metagenomic analysis, we show that predicted Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways responsible for macro- and micronutrient uptake are significantly depleted under Zn deficiency; along with concomitant decreases in beneficial short chain fatty acids, such depletions may further preclude optimal host Zn availability. We also identify several candidate microbes that may play a significant role in modulating the bioavailability and utilization of dietary Zn during prolonged deficiency. Our results are the first to characterize a unique and dysbiotic cecal microbiota during Zn deficiency, and provide evidence for such microbial perturbations as potential effectors of the Zn deficient phenotype.
Experiment setup
Upon hatching, chicks were randomly allocated into two treatment groups on the basis of body weight and gender (aimed to ensure equal distribution between groups, n = 6): 1. Zn(+): 42 µg/g zinc; 2. Zn(−): 2.5 µg/g zinc.
Research is published:
http://www.mdpi.com/2072-6643/7/12/5497/htm
2015-06-08 | ST000190 | MetabolomicsWorkbench
Project description:Phase II randomized trial to investigate whether supplementation of zinc decreases the incidence of HFSR that occurs after treatment of tyrosine kinase inhibitor, regorafenib.
| 2301575 | ecrin-mdr-crc