Rattus norvegicus
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ABSTRACT:
PROVIDER: PRJNA281878 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Transcriptional profiling of mouse liver after short-term in vivo exposure (up to 56 days) of C57BL-mice to carcinogenic and non-carcinogenic chemicals
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Project description:Transcriptional profiling of microRNAs after short-term exposure of CD1-mice to carcinogenic and non-carcinogenic chemicals
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Project description:The carcinogenic potential of chemicals is currently evaluated with rodent life-time bioassays, which are time consuming, and expensive with respect to cost, number of animals and amount of compound required. Since the results of these 2-year bioassays are not known until quite late during development of new chemical entities, and since the short-term test battery to test for genotoxicity, a characteristic of genotoxic carcinogens, is hampered by low specificity, the identification of early biomarkers for carcinogenicity would be a big step forward. Using gene expression profiles from the livers of rats treated up to 14 days with genotoxic and non-genotoxic carcinogens we previously identified characteristic gene expression profiles for these two groups of carcinogens. We have now added expression profiles from further hepatocarcinogens and from non-carcinogens the latter serving as control profiles. We used these profiles to extract biomarkers discriminating genotoxic from non-genotoxic carcinogens and to calculate classifiers based on the support vector machine (SVM) algorithm. These classifiers then predicted a set of independent validation compound profiles with up to 88% accuracy, depending on the marker gene set. We would like to present this study as proof of the concept that a classification of carcinogens based on short-term studies may be feasible.
2016-04-27 | GSE68110 | GEO
Project description:Mycotoxin citrinin (CTN) is a secondary metabolite of fungi, becoming a contaminant widely found in foods, feeds, and fermented health supplements. CTN is known to disrupt microtubule and chromosome arrangement at high dose (50 - 150 μM), but the toxicological effect of CTN long-term exposure has not been clearly studied. To investigate the molecular mechanisms of genotoxic, clastogenic, and carcinogenic effects of CTN, RNA-seq was performed on HEK293 cells exposed to chronic 20 μM CTN treatment (3 days for short-term and 30 days for long-term). The transcriptomic profile may reveal some underlying mechanisms regarding chronic carcinogenic potential of CTN, providing information for risk assessment of CTN-contaminated grains and its commercial food products.
2023-03-01 | GSE218082 | GEO
Project description:Addictive drugs including opioids activate signal transduction pathways that regulate gene expression in the brain. However, changes in CNS gene expression following morphine exposure are poorly understood. We studied the effect of short- and long-term morphine treatment on gene expression in the hypothalamus and pituitary using genome-wide DNA microarray and real-time reverse transcriptase polymerase chain reaction (RT-PCR) analyses. In the hypothalamus, we found that short-term morphine administration up-regulated (at least 2-fold) 39 genes and down-regulated six genes. Long-term morphine administration up-regulated 35 genes and down-regulated 51 hypothalamic genes. In the pituitary, we found that short-term morphine administration up-regulated (at least 2-fold) 110 genes and down-regulated 29 genes. Long-term morphine administration up-regulated 85 genes and down-regulated 37 pituitary genes. Strikingly, microarray analysis uncovered several genes involved in food intake (neuropeptide Y, agouti-related protein, and cocaine and amphetamine-regulated transcript) whose expression was strongly altered by morphine exposure in either the hypothalamus or pituitary. Subsequent RT-PCR analysis confirmed similar gene regulation of noteworthy genes in these regions. Finally, we found functional correlation between morphine-induced alterations in food intake and regulations of genes involved in this process. Changes in genes related to food intake may uncover new pathways related to some of the physiological effects of opioids. Keywords: Comparative treatment versus placebo 8 samples analyzed: 4 from hypothalamus (2 biological replicates and 2 dye swaps) and 4 from pituitary (2 biological replicates and 2 dye swaps) 8 samples analyzed: 4 from hypothalamus short term treatment (2 biological replicates and 2 dye swaps) and 4 hypothalamus long term treatment (2 biological replicates and 2 dye swaps)
2008-09-30 | E-GEOD-9525 | biostudies-arrayexpress
Project description:Addictive drugs including opioids activate signal transduction pathways that regulate gene expression in the brain. However, changes in CNS gene expression following morphine exposure are poorly understood. We studied the effect of short- and long-term morphine treatment on gene expression in the hypothalamus and pituitary using genome-wide DNA microarray and real-time reverse transcriptase polymerase chain reaction (RT-PCR) analyses. In the hypothalamus, we found that short-term morphine administration up-regulated (at least 2-fold) 39 genes and down-regulated six genes. Long-term morphine administration up-regulated 35 genes and down-regulated 51 hypothalamic genes. In the pituitary, we found that short-term morphine administration up-regulated (at least 2-fold) 110 genes and down-regulated 29 genes. Long-term morphine administration up-regulated 85 genes and down-regulated 37 pituitary genes. Strikingly, microarray analysis uncovered several genes involved in food intake (neuropeptide Y, agouti-related protein, and cocaine and amphetamine-regulated transcript) whose expression was strongly altered by morphine exposure in either the hypothalamus or pituitary. Subsequent RT-PCR analysis confirmed similar gene regulation of noteworthy genes in these regions. Finally, we found functional correlation between morphine-induced alterations in food intake and regulations of genes involved in this process. Changes in genes related to food intake may uncover new pathways related to some of the physiological effects of opioids. Keywords: Comparative treatment versus placebo
2008-10-01 | GSE9525 | GEO
Project description:Liver tumors in rodents are frequently induced by non-genotoxic carcinogens. These hepatocarcinogens generally activate hepatic nuclear receptors (e.g., CAR and PXR), resulting in a cascade of signals causing modifications in the expression of genes responsible for several processes involved in carcinogenesis. Evaluation of the carcinogenic potential of chemicals is a regulatory requirement but is time-consuming and expensive. Consequently, several short-term in vivo and in vitro approaches, using molecular tools, have been proposed as predictive models for non-genotoxic hepatocarcinogens. The objective of our study was to discriminate between chemicals that are either non-genotoxic hepatocarcinogens or merely hepatotoxicants and also between CAR and PXR modulators on the basis of their gene expression profiles. Thus, we treated rats for seven days with the hepatoxicants, diclofenac and diazepam, or with several CAR and PXR modulators, which were mainly hepatocarcinogens. Different hepatic gene expression profiles were obtained not only between the hepatotoxicants and the non-genotoxic hepatocarcinogens but also between the CAR activators phenobarbital, phenytoin and 1,1-bis-(4-chlorophenyl)-2,2-dichloroethene which were grouped together, and the two PXR activators pregnenolone 16α-carbonitrile and clotrimazole. Diethylstilbestrol had an expression profile that was quite distinct from the other PXR activators, suggesting that this compound is certainly not a classic PXR modulator. Moreover, some differences were observed between phenytoin (not considered as a hepatocarcinogen), and the other two CAR activators. Our data therefore indicate that discrimination is possible between hepatocarcinogens and hepatotoxicants, between CAR and PXR modulators and also between compounds within the same class of modulators using a short-term transcriptomic approach. CAR or PXR inducers were administered in suspension to rats (7 weeks old at start of treatment) by oral gavage at a daily dose for 7 consecutive days. Treatment-related changes in gene expression were determined in the liver using whole genome oligonucleotide microarrays.
2013-07-31 | E-GEOD-39350 | biostudies-arrayexpress
Project description:We used microarrays to unveil the gene expression alterations upon short-term HFD administration We found that short-term HFD administration impacts hepatic lipid biosynthesis and redox status
2017-08-01 | GSE94867 | GEO
Project description:A comprehensive time-course experiment of Pi-starved plants was undertaken, spanning medium (3 and 7 days), and long-term (21 days up to 52 days) Pi deprivation (âPi), as well as both short term (1 and 3 days) and long-term (31 days) recovery. The 52 days time point consisting of 21 days starvation +31 days recovery enabled investigation of the effects of long term resupply on Pi starved plants, and coincided with the emergence of the first panicles and grains. Pre-germinated rice seedlings were grown for 14 days in Pi sufficient conditions (0.32 mM Pi) before being transferred to either Pi sufficient (0.32 mM Pi) or Pi deficient (0 mM Pi) media for 21 days. After 21 days of Pi deficient treatment, half of the plants were either maintained under Pi deficient conditions or re-supplied with Pi (0.32 mM) for 1, 3 or 31 days. To confirm the effectiveness of the Pi starvation and resupply treatments, physiological and molecular analyses were performed.
2015-07-31 | E-MTAB-4334 | biostudies-arrayexpress
Project description:Liver tumors in rodents are frequently induced by non-genotoxic carcinogens. These hepatocarcinogens generally activate hepatic nuclear receptors (e.g., CAR and PXR), resulting in a cascade of signals causing modifications in the expression of genes responsible for several processes involved in carcinogenesis. Evaluation of the carcinogenic potential of chemicals is a regulatory requirement but is time-consuming and expensive. Consequently, several short-term in vivo and in vitro approaches, using molecular tools, have been proposed as predictive models for non-genotoxic hepatocarcinogens. The objective of our study was to discriminate between chemicals that are either non-genotoxic hepatocarcinogens or merely hepatotoxicants and also between CAR and PXR modulators on the basis of their gene expression profiles. Thus, we treated rats for seven days with the hepatoxicants, diclofenac and diazepam, or with several CAR and PXR modulators, which were mainly hepatocarcinogens. Different hepatic gene expression profiles were obtained not only between the hepatotoxicants and the non-genotoxic hepatocarcinogens but also between the CAR activators phenobarbital, phenytoin and 1,1-bis-(4-chlorophenyl)-2,2-dichloroethene which were grouped together, and the two PXR activators pregnenolone 16α-carbonitrile and clotrimazole. Diethylstilbestrol had an expression profile that was quite distinct from the other PXR activators, suggesting that this compound is certainly not a classic PXR modulator. Moreover, some differences were observed between phenytoin (not considered as a hepatocarcinogen), and the other two CAR activators. Our data therefore indicate that discrimination is possible between hepatocarcinogens and hepatotoxicants, between CAR and PXR modulators and also between compounds within the same class of modulators using a short-term transcriptomic approach.
2013-07-31 | GSE39350 | GEO