Metabolomics Workbench ST000330 - GNPS - Effects of Zinc on GI tract metabolites (Part 1: Esophagus)
Ontology highlight
ABSTRACT:
INSTRUMENT(S): Q-TOF - NEGATIVE, Q-TOF - POSITIVE
ORGANISM(S): Mus Musculus
SUBMITTER: 
Oliver Fiehn
PROVIDER: MSV000082696 | GNPS | Thu Aug 02 17:07:00 BST 2018
REPOSITORIES: GNPS
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Project description:Weanling littermates Cox-2-/- and Cox-2+/+ (WT) mice were fed a zinc-deficient (ZD) or zinc-sufficient (ZS) diet to form 4 groups, namely, ZD:Cox-2-/- (n=4), ZD:WT (n=4), ZS:Cox-2-/- (n=4) and ZS:WT (n=4). After 8 weeks, ZD mouse forestomach evidenced increased cell proliferation as demonstrated by increased proliferating cell nuclear antigen [PCNA] labeling. The mice were sacrificed and forestomachs isolated. Forestomach epithelia were prepared by using a blade to strip off the submucosal and muscularis layers under the guidance of a dissecting microscope. We performed microarray analysis on individual RNA samples prepared from 4 mice from each of the following 4 groups: ZS:Cox-2-/-, ZS:WT, ZD:Cox-2-/- and ZD:WT mice (n=4/group), using GeneChipï¾® Mouse Genome 430 2.0 Array (Affymetrix, Santa Clara, CA). All RNA samples displayed intact ribosomal RNA 18S and 28S bands as determined by the Agilent 2100 Bioanalyzer. Five micrograms of total RNA was reverse transcribed into cDNA followed by in vitro transcription and labeling to produce biotin-labeled cRNA using IVT Labeling Kit. The labeled cRNA was hybridized to the array, followed staining with streptavidin-phycoerythrin. The distribution of fluorescent material on the oligonucleotide probes sets was obtained using GeneArray Scanner
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Project description:Zinc deficiency during pregnancy and postnatal life can adversely affect the health and predispose to an increased risk of developing human diseases at adulthood. The present study was designed to evaluate whether dietary zinc deficiency or supplementation during the pregnancy, lactation and juvenile stages interferes with the development of mammary tumors induced by 7,12-dimethylbenzanthracene (DMBA) in female Sprague-Dawley (SD) rats. Pregnant females SD were allocated into three groups: dams received diets containing adequate (35 mg/Kg chow), deficient (3 mg/Kg chow) or supplemented (180 mg/Kg chow) zinc levels during gestational day 10 (GD 10) until the litters weaning. Female offspring were allocated into three groups and received the same diets as their dams until postnatal day (PND) 51. At PND 51, females SD (n=16 each group) received a single dose of DMBA (50 mg/kg, ig) for initiation of mammary carcinogenesis, adequate zinc diets and were euthanized at PND 180. Tumors samples were collected and processed for histological evaluation and microarray analysis. Dietary zinc deficiency induced a significant reduction in female offspring body weight evolution at parturition, weaning and pubertal phases. At late in life, the early in life dietary zinc deficiency or supplementation did not alter the latency, incidence, multiplicity and volume or histological types of mammary tumors in relation to the adequate zinc group, and changed the expression of a small amount of genes. The present findings indicate that early-in life dietary zinc deficiency or supplementation did not significantly modify the susceptibility to development of mammary tumors induced by DMBA.
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Dynamic model of iron distribution in mice. This model attempts to fit the radioiron tracer data from Lopes et al. 2010 for mice fed iron deficient and rich diets by adjusting the rate of iron intake (vDiet) and the hepcidin synthesis rate (vhepcidin) independently for each experiment. All other parameters are those that provide the best fit for the adequate diet.
This model includes the radioiron tracer species.
Differences in parameter values between deficient, rich, and adequate diets:
Diet
vDiet
vhepcidin
Adequate
0.00377422
1.7393e-08
Deficient
0
8.54927e-09
Rich
0.00415624
2.30942e-08
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