Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Expression data from mouse liver on multisetp-exposure to ethylbenzene

ABSTRACT: The processes involved in the adaptation of animals to environmental factors such as chemicals have not yet been fully elucidated. We focused on the adaptive potential of the mouse liver against hepatotoxic chemical-induced injury. We used microarrays to determine genes with adaptive transcriptional regulation against ethylbenzene, hepatotoxic chemical, on multistep-exposure. Four animal groups received the following treatments: phosphate-buffered saline (PBS) followed by PBS (P+P), ethylbenzene followed by PBS (E+P), PBS followed by ethylbenzene (P+E), and ethylbenzene followed by ethylbenzene (E+E). For the first exposure, ethylbenzene (7 mmol kg-1) or PBS (equivalent volume to ethylbenzene) was intraperitoneally injected twice at a 24 h interval. After 7 days of normal feeding, each animal group was treated with ethylbenzene (7 mmol kg-1) or PBS as the secondary exposure. The mice were sacrificed 5 h after the secondary exposure for RNA extraction and hybridization on Affymetrix. The number of mice of each group is as follows, P+P, E+P = 3. P+E, E+E = 5. Specimens from mice of each group were pooled, and 10 μg RNA from each pool was used for cRNA synthesis.

ORGANISM(S): Mus musculus

SUBMITTER: Minori Dateki

PROVIDER: E-GEOD-22535 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:Since xenobiotics enter the organism via the liver, hepatocytes must cope with numerous perturbations. In particular, exposure to hepatotoxic agents resulting in liver injury triggers a strong alteration in gene expression. The contribution of these transcriptional regulatory networks to the propagation of injury (i.e. by modulation of metabolic pathways, inflammation, proliferation) are not fully understood. Therefore, we conducted a time-resolved gene array study on mouse liver after exposure to a single intraperitoneal injection of the hepatotoxic compound carbon tetrachloride (CCl4). This model induces a transient injury which reaches its maximum between 2 to 3 days after injection, followed by a precise regenerative response. The experiment included early time points (i.e. 2 and 8h) and late time points (1 to 16 days) to cover the initial events induced by CCl4 metabolization and cell stress, and the regenerative phase between 2-6 days after intoxicaiton. C57BL/6N male mice (8-12 weeks old) were obtained from Charles Rivers (Sulzfeld, Germany). The local Ethics committee approved the experiments. 4-5 mice were used for each time point. Mice received a single intraperitoneal injection of CCl4 (1.6 g/kg body weight) dissolved in 0.5 ml olive oil. The liver tissue was collected after 2h, 8h, and 1, 2, 4, 6, 8 and 16 days following CCl4 administration. As control, mice received 0.5 ml of olive oil intraperitonealy for 1 or 8 days. Healthy liver was collected from untreated mice. At the indicated time points, mice were anesthetized and blood was collected from the heart with a 25 gauge needle, using EDTA as anticoagulant, for analysis of the liver transaminases GOT and GPT in serum. Afterwards, the liver was resected, washed in ice cold PBS and sectioned for further analysis. Liver tissue sections of about 0.5 cm2 were snap frozen in liquid nitrogen and stored at -80ﾰC for subsequent isolation of proteins or RNA. RNA was isolated from mouse liver tissue using the Phenol/Chloroform method (Trizolﾮ, Qiagen, Hilden, Germany) according to the manufacturerﾒs instructions. RNA concentration and integrity were determined spectrophotometrically in a Nanodropﾮ2000 (ThermoScientific, Waltham MA, USA) and in a Bioanalyzerﾮ (Agilent, Waldbronn, Germany), respectively.

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Expression data from mouse liver on multisetp-exposure to ethylbenzene

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