Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Transcriptome analysis of E. coli in M9 minimal media supplemented with propylene glycol or glycerol

ABSTRACT: The aim of this study is to investigate the changes of global gene expression in E. coli during a carbon source shift. Expression profiling of an evolved strain of E. coli K12 MG1655 grown in M9 minimal media supplemented with propylene glycol or glycerol. A six chip study under two separate culture conditions

ORGANISM(S): Escherichia coli str. K-12 substr. MG1655

SUBMITTER: Bernhard Palsson

PROVIDER: E-GEOD-34631 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:Propylene glycol (PG) is a common carrier in e-vapor formulations and its properties have been extensively studied. In this 13-week subchronic nose-only inhalation study, Sprague Dawley rats were exposed to filtered air (sham control group), propylene glycol/water (PG/W; 90:10) or a propylene glycol/vegetable glycerin/water (PG/VG/W; 50:40:10) reference. The reference containing vegetable glycerin group was added at the high dose to observe any changes that might be associated with a carrier more in line with e-vapor products. The objectives of this study were to increase the PG exposure above the concentrations tested by Suber et al. and use a systems toxicology analysis of lung tissue to further our understanding of molecular events after PG exposures (Suber et al. 1989). Macroscopic examinations at necropsy as well as terminal organ weights revealed no observations that were associated with exposure to PG/W or reference. Food consumption and body weights were unaffected by PG/W or reference when compared to the sham. No exposure related alterations were observed in serum chemistry, hematology, coagulation, urinalysis or BALF cytology and clinical chemistry. Although clinical observations of dried red material around the nose in the high dose PG/W group were reported, histopathology of the nasal cavity showed no nasal hemorrhaging. There were non-adverse PG/W and reference related findings of minimal mucus cell hyperplasia noted in nasal cavity section II. These findings were considered non-adverse as they were also found to a lesser extent in the filtered air controls. No other exposure-related findings were noted in the primary or recovery necropsies. A systems toxicology analysis on lung tissue showed no statistically-significant differentially expressed transcripts or proteins compared to the sham group. The endpoints measured from the PG/W high dose group did not differ significantly from those in the more common carrier PG/VG/W. Accordingly, the highest PG exposure (5 mg/L, 6 hrs/day) was regarded as the no observed adverse effect concentration (NOAEC), corresponding to a PG delivered dose of 1,152 mg/kg/day in rats.

Project description:Glucocorticoids are a well recognized and common cause of muscle atrophy. Glucocorticoid-induced atrophy can be prevented by testosterone, but the molecular mechanisms underlying such protection have not been described. Thus, the global effects of testosterone on dexamethasone-induced changes in gene expression were evaluated in rat gastrocnemius muscle using Affymetrix 230_2 DNA microarrays. Gene expression was analyzed after 7 days administration of dexamethasone, dexamethasone plus testosterone, or vehicle. Effects of these agents on weights of gastrocnemius muscles from these animals has been reported (1. Zhao W, Pan J, Zhao Z, Wu Y, Bauman WA, and Cardozo CP. Testosterone protects against dexamethasone-induced muscle atrophy, protein degradation and MAFbx upregulation. J Steroid Biochem Mol Biol 110: 125-129, 2008.) Dexamethasone changed expression of 876 probe sets by at least 2-fold, of which 474 probe sets were changed by at least two fold in the opposite direction in the dexamethasone plus testosterone group (genes in opposition). Major biological themes represented by genes in opposition included IGF-1 signaling, protein synthesis, myogenesis and muscle development, and ubiquitin conjugases and ligases. Testosterone blocked increased expression of DDIT4 and eIF4EBP1, FOXO1 and of the p85 regulatory subunit of the IGF-1 receptor, while preventing decreased expression of IRS-1. Testosterone blocked decreased expression of LXR and suppressed upregulation of C/EBP beta and delta. Testosterone prevented increase expression of Cdkn1A (p21) and decrease expression of cyclins B and D, as well as many other changes that would be expected to reduce cell cycle progression. Testosterone prevented increased expression of muscle development factors Csrp3 and Mbn1 and blocked reduced expression of Wnt4. These data suggest that testosterone blocks multiple changes in gene expression that, collectively, would otherwise downregulate molecular signals that promote protein synthesis and muscle hypertrophy and that stimulate muscle protein catabolism. Experiment Overall Design: Rats (250 g males) were administered dexamethasone (0.7 mg/kg/day) alone or with testosterone (20 mg/kg/day) dissolved in vehicle (propylene glycol) by continuous infusion (Alzet pumps) for 7 days. Control animals were administered vehicle only. Gene expression was compared among the 3 groups at 7 days using one chip per animal, 3 animals per group.

Project description:The main constituents of electronic cigarette liquids are nicotine, propylene glycol (PG), and vegetable glycerin (VG), together with distilled water and flavors. To assess the toxicity of PG/VG mixtures with and without nicotine as basic components of liquids used in e-cigarettes, a 90-day rat inhalation study according to the Organization for Economic Co-operation and Development test guideline 413 was conducted. Sprague-Dawley (SD) rats were nose-only exposed, 6?h/day, 5 days/week to filtered air, or nebulized vehicle (saline), or three concentrations of PG/VG (0.174 mg PG/l + 0.210 mg VG/l; 0.520 mg PG/l + 0.630 mg VG/l; 1.520 mg PG/l + 1.890 mg VG/l) ï¿½ with (test item) and without (reference item) 23 ï¿½g nicotine/L. Standard toxicological endpoints were complemented by molecular analyses using transcriptomics, proteomics, and lipidomics. Compared to vehicle exposure, the tested PG/VG aerosols showed only very limited biological effects with no signs of toxicity, both for the standard toxicological endpoints (e.g., histopathology, clinical chemistry) and the systems toxicological analyses (transcriptomics, proteomics, and lipidomics). The addition of nicotine to the PG/VG aerosols (23 ï¿½g/l) resulted in effects in line with nicotine effects in previous studies. These included up-regulation of xenobiotic enzymes (Cyp1a1 and Fmo3) in the lung and metabolic effects, e.g., reduction in serum lipid concentrations and changes in the expression of metabolic enzymes in the liver. Signs of a generalized stress response to nicotine exposure such as decreased thymus weights were observed; and likely, a subset of the observed metabolic alterations was interlinked with this generalized stress response. Under the conditions of this 90-day SD rat inhalation study, no toxicologically relevant effects of PG/VG aerosols (up to 1.520 mg PG/l + 1.890 mg VG/l) were observed, and the no observed adverse effect level (NOAEL) for PG/VG/nicotine was determined to be 438/544/6.7 mg/kg/day. Further the study demonstrated how complementary systems toxicology analyses can reveal, also in the absence of observable adverse effects, subtoxic and adaptive responses to pharmacologically active compounds such as nicotine.

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Transcriptome analysis of E. coli in M9 minimal media supplemented with propylene glycol or glycerol

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