Gene expression profiling of responses to dimethylarsinic acid in female F344 rat urothelium

Sen, Banalata; Wang, Amy; Hester, Susan; Robertson, John L.; Wolf, Douglas C.

doi:10.1016/j.tox.2005.07.008

Cited by 27 publications

(15 citation statements)

References 38 publications

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“…The utility of gene expression profiling in hazard identification has been examined for a limited number of chemicals, including dibutyl phthalate and acetaminophen (Euling et al, 2011;Kienhuis et al, 2011;Makris et al, 2010). Toxicogenomic profiles of alachlor exposure in rat olfactory mucosa (Genter et al, 2002) and dimethylarsenic (DMA) exposure in human cultured bladder cells and rat bladder epithelium (Sen et al, 2005; US EPA, 2005) have also Table 3 Comparison of CBNP profiles with lung disease models using functional analysis for genes in common (grey) and genes unique to CBNP (black). provided useful information for two final assessments of acetochlor and arsenicals (US EPA, 2004.…”

Section: Hazard Identification Mode Of Action and Prediction Of Apicmentioning

confidence: 99%

Gene expression profiling to identify potentially relevant disease outcomes and support human health risk assessment for carbon black nanoparticle exposure

et al. 2013

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New approaches are urgently needed to evaluate potential hazards posed by exposure to nanomaterials. Gene expression profiling provides information on potential modes of action and human relevance, and tools have recently become available for pathway-based quantitative risk assessment. The objective of this study was to use toxicogenomics in the context of human health risk assessment. We explore the utility of toxicogenomics in risk assessment, using published gene expression data from C57BL/6 mice exposed to 18, 54 and 162 μg Printex 90 carbon black nanoparticles (CBNP). Analysis of CBNP-perturbed pathways, networks and transcription factors revealed concomitant changes in predicted phenotypes (e.g., pulmonary inflammation and genotoxicity), that correlated with dose and time. Benchmark doses (BMDs) for apical endpoints were comparable to minimum BMDs for relevant pathway-specific expression changes. Comparison to inflammatory lung disease models (i.e., allergic airway inflammation, bacterial infection and tissue injury and fibrosis) and human disease profiles revealed that induced gene expression changes in Printex 90 exposed mice were similar to those typical for pulmonary injury and fibrosis. Very similar fibrotic pathways were perturbed in CBNP-exposed mice and human fibrosis disease models. Our synthesis demonstrates how toxicogenomic profiles may be used in human health risk assessment of nanoparticles and constitutes an important step forward in the ultimate recognition of toxicogenomic endpoints in human health risk. As our knowledge of molecular pathways, dose-response characteristics and relevance to human disease continues to grow, we anticipate that toxicogenomics will become increasingly useful in assessing chemical toxicities and in human health risk assessment.

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Section: Hazard Identification Mode Of Action and Prediction Of Apicmentioning

confidence: 99%

Gene expression profiling to identify potentially relevant disease outcomes and support human health risk assessment for carbon black nanoparticle exposure

et al. 2013

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“…Previous microarray studies on arsenic were mainly performed in vitro using human or murine cell lines (4,6,21,22,45,64,66,67) and yeast (29), while in vivo studies typically involved chronic exposure to arsenic (37,62,63). A recent study investigated subacute in vivo effects of dimethylarsinic acid on gene expression profiles of rat urothelium (48). Although many arsenic-induced, differentially expressed genes have been identified, there are no data on in vivo kinetics evaluated by the microarray approach on the adaptive response of a specific targeted organ, such as liver; undoubtedly, these data from microarray analyses should aid further understanding of arsenic mechanisms of toxicity resulting in pathology.…”

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confidence: 99%

Transcriptome kinetics of arsenic-induced adaptive response in zebrafish liver

Lam

Winata

Tong

et al. 2006

Physiological Genomics

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-Arsenic is a prominent environmental toxicant and carcinogen; however, its molecular mechanism of toxicity and carcinogenicity remains poorly understood. In this study, we performed microarray-based expression profiling on liver of zebrafish exposed to 15 parts/million (ppm) arsenic [As(V)] for 8 -96 h to identify global transcriptional changes and biological networks involved in arsenic-induced adaptive responses in vivo. We found that there was an increase of transcriptional activity associated with metabolism, especially for biosyntheses, membrane transporter activities, cytoplasm, and endoplasmic reticulum in the 96 h of arsenic treatment, while transcriptional programs for proteins in catabolism, energy derivation, and stress response remained active throughout the arsenic treatment. Many differentially expressed genes encoding proteins involved in heat shock proteins, DNA damage/repair, antioxidant activity, hypoxia induction, iron homeostasis, arsenic metabolism, and ubiquitin-dependent protein degradation were identified, suggesting strongly that DNA and protein damage as a result of arsenic metabolism and oxidative stress caused major cellular injury. These findings were comparable with those reported in mammalian systems, suggesting that the zebrafish liver coupled with the available microarray technology present an excellent in vivo toxicogenomic model for investigating arsenic toxicity. We proposed an in vivo, acute arsenic-induced adaptive response model of the zebrafish liver illustrating the relevance of many transcriptional activities that provide both global and specific information of a coordinated adaptive response to arsenic in the liver. microarray expression profiling; arsenic toxicity; oxidative stress; fish toxicogenomics ARSENIC IS AN IMPORTANT and ubiquitous environmental toxicant, and the risk of arsenic poisoning in humans is a public health issue worldwide (1,23,27,46,54). In addition, arsenic is classified as a human carcinogen based on several epidemiological studies showing an association of arsenic exposure with cancers in lung, bladder, kidney, and liver (33, 54). Aside from cancers, arsenic ingestion is also associated with other human diseases such as blackfoot disease, atherosclerosis, hypertension, diabetes mellitus, skin lesions, and liver injury (19,20,37,54,62). Despite these findings and the fact that arsenic is the most extensively studied of the metals and metalloids in drinking water, the molecular mechanisms of arsenic toxicity and carcinogenicity are poorly understood (34,46). This is partly due to the difficulty of inducing cancer with arsenic in animal models and the complex effects induced by arsenic through a variety of mechanisms that influence numerous signal transduction pathways, as these effects vary depending on cell type, dosage, and form of arsenic used (7, 60). Thus many different modes of action have been proposed, and these include both genotoxic and nongenotoxic effects (33,34,46). Some of the genotoxic effects include induction of chromosomal abnor...

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“…We found that the number of genes altered by diuron after 7 days of exposure followed a dose-response relationship, although no significant morphological lesions were observed in any diuron treatment group using LM and only a minimal response was seen under SEM. Other studies that have investigated dose-response effects of toxicants using integrated transcriptomics and classic toxicological endpoints have also reported that transcriptional changes may be observed in the absence of morphological or clinical manifestations (Sen et al, 2005;Nesnow et al, 2009;Ludwig et al, 2011). Unsupervised analysis (PCA) revealed that the gene expression profile of the 2500 ppm group was clearly separated from the profiles of other dose levels, indicating that even after 7 days the carcinogenic dose elicited a transcriptional response that was distinguishable from the other doses.…”

Section: Discussionmentioning

confidence: 99%

Dose and temporal effects on gene expression profiles of urothelial cells from rats exposed to diuron

Ihlaseh-Catalano

Bailey²,

Cardoso

et al. 2014

Toxicology

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Gene expression profiling of responses to dimethylarsinic acid in female F344 rat urothelium

Cited by 27 publications

References 38 publications

Gene expression profiling to identify potentially relevant disease outcomes and support human health risk assessment for carbon black nanoparticle exposure

Gene expression profiling to identify potentially relevant disease outcomes and support human health risk assessment for carbon black nanoparticle exposure

Transcriptome kinetics of arsenic-induced adaptive response in zebrafish liver

Dose and temporal effects on gene expression profiles of urothelial cells from rats exposed to diuron

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