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ABSTRACT:
PROVIDER: PRJNA108345 | ENA |
REPOSITORIES: ENA
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Project description:Aflatoxin B1 treatment with 10,000 ppm for 2 h
| PRJNA108991 | ENA
Project description:Aflatoxin G1 treatment with 10,000 ppm for 2 h
| PRJNA108993 | ENA
Project description:Deoxynivalenol treatment with 10,000 ppm for 2 h
| PRJNA108247 | ENA
Project description:Perfluorooctanoic acid (PFOA) is a potent hepatocarcinogen and peroxisome proliferator (PP) in rodents. Humans are not susceptible to peroxisome proliferation and are thought to be refractory to carcinogenesis by PFOA and other PPs. However, previous studies with rainbow trout have shown that they are also insensitive to peroxisome proliferation by the PP, dehydroepiandrosterone (DHEA), but are still susceptible to enhanced hepatocarcinogenesis after chronic exposure. In this study, we determined whether PFOA is also a tumor promotor in trout and then examined hepatic gene expression profiles to further investigate possible mechanisms of action. Trout were initiated as fry to the hepatocarcinogen, aflatoxin B1, and then fed 200-1800 ppm PFOA in the diet for 30 weeks. Two structurally diverse PPs, clofibrate (CLOF) and DHEA, were included for comparison. Hepatic gene expression profiles were subsequently examined in animals exposed to similar doses of PFOA, DHEA and CLOF along with 5 ppm 17β-estradiol (E2; a known tumor promotor) in the diet. PFOA (1800 ppm) and DHEA treatments resulted in enhanced liver tumor incidence and multiplicity while CLOF showed no effect. Carcinogenesis seemed independent of peroxisome proliferation as no induction of peroxisomal β-oxidation and catalase activity were observed. Alternately, plasma VTG was elevated in fish fed PFOA and DHEA suggesting that estrogenic mechanisms may play a role. Both tumor promotors, PFOA and DHEA, resulted in strong correlation of transcriptional profiles with E2 by Pearson correlation (R=0.81 and 0.78, respectively). In comparison, CLOF regulated no genes in common with E2. Overall, these data suggest that the tumor promoting activities of DHEA and PFOA in trout are independent of peroxisome proliferation and may involve estrogenic mechanisms. Juvenile trout, 12-18 months old, were fed experimental diets containing 500 or 1800 ppm PFOA, 1800 ppm CLOF, 750 ppm DHEA, 5 ppm E2 or 0.15 % dimethyl sulfoxide vehicle control for 14 days. Liver samples were collected for microarray analysis. Hybridizations were performed using standard reference design with dye-swapping. For each sample, equal amounts of RNA (µg) were pooled from five fish per tank for every treatment (n=3 biological replicates per treatment). cDNA from two of the three biological replicates was dye-swapped and hybridized to two slides as technical replicates (5 arrays per treatment).
2007-08-31 | E-GEOD-7837 | biostudies-arrayexpress
Project description:The evaluation of the toxicity of Aflatoxin B1 using yeast gene expressions. Two yeast strains; parental BY4743 and PTC1 mutant, were used for this study. SDS was used to raise the penetration of the yeast cell membrane. Two conditions are compared with three replicates each. Both strains were grown in 0.01% SDS containing YPD media or 0.01% SDS, 25 ppm ABF1 containing YPD media. Publication can be found at http://www.cbi.or.jp/cbi/CBIj/vol9/9_94-E.pdf.
2010-04-12 | E-GEOD-17367 | biostudies-arrayexpress
Project description:Crlj:CD1(ICR) female mice were fed diets containing 0 ppm (control), 5000 ppm permethrin, and 5000 ppm clofibrate for periods of 2 weeks. We used microarrays to evaluate gene expression profiling in mouse liver at the early phase of treatment with permethrin or clofibrate.
2019-12-10 | GSE124081 | GEO
Project description:Indole-3-carbinol (I3C) and 3,3’-diindolylmethane (DIM), a primary I3C derivative in vivo, are known dietary chemopreventive agents also available as dietary supplements. However, I3C has been found to act as a tumor promoter in rat (multi-organ) and trout (liver) models. I3C and DIM were previously found to be estrogenic in trout liver based on toxicogenomic profiles. In this study, we compare the post-initiation effects of DIM and 17β-estradiol (E2) on aflatoxin B1 (AFB1)-induced hepatocarcinogenesis in trout. Trout were initiated as embryos with 50 ppb AFB1, fed control diet for three months followed by diets containing 0, 120 or 400 ppm DIM or 5 ppm E2 for 18 weeks before returning all groups to control diet. Tumor incidence was determined 13 months later and found to be significantly elevated in AFB1-initiated trout fed either 400 ppm DIM or 5 ppm E2 compared to control animals. To evaluate the mechanism of tumor enhancement, hepatic gene expression profiles were examined in animals fed promotional diets during the course of tumorigenesis and in hepatocellular carcinomas (HCCs) of initiated animals using a rainbow trout 70-mer custom oligonucleotide array. We demonstrate that DIM alters gene expression profiles similar to E2 in liver samples during tumorigenesis and in HCC tumors. Further, HCCs from animals on DIM and E2 promotional diets had a transcriptional signature indicating decreased invasive or metastatic potential compared to HCCs from control animals. Overall, these findings are the first to demonstrate tumor promotion by DIM. They confirm the importance of estrogenic signaling in the mechanism of promotion by dietary indoles in trout liver and indicate a possible dual effect that enhances tumor incidence and decreases potential for metastasis. Keywords: treatment effect
2006-12-31 | GSE5643 | GEO
Project description:Male Fischer rats were fed a control diet or a diet supplemented with 50, 500 or 1000 ppm Phenobarbital. The 500 and 1000 ppm PB doses induced a transient hyperplasia and a sustained hepatomegaly in treated animals. The animals were sacrificed and liver miRNAome was profiled in three animals per group after 1, 3, 7, and 14 days of treatment. The aim was to investigate the time and dose dependent effects of phenobarbital treatment on the liver miRNAome
2013-07-03 | GSE48489 | GEO