Dataset Information

Cytenamide-1,4-dioxane (2/1).

ABSTRACT: IN THE CRYSTAL STRUCTURE OF THE TITLE COMPOUND [SYSTEMATIC NAME: 5H-dibenzo[a,d]cyclo-hepta-triene-5-carboxamide-1,4-dioxane (2/1)], 2C(16)H(13)NO·C(4)H(8)O(2), the cytenamide mol-ecules form a hydrogen-bonded R(2) (2)(8) dimer. The solvent mol-ecule is located between two adjacent cytenamide dimers and forms N-H⋯O hydrogen bonds with one cytenamide mol-ecule from each dimer.

SUBMITTER: Johnston A

PROVIDER: S-EPMC2961860 | biostudies-literature | 2008 Jun

REPOSITORIES: biostudies-literature

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Cytenamide-1,4-dioxane (2/1).

Johnston Andrea A Florence Alastair J AJ Fabbiani Francesca J A FJ Shankland Kenneth K Bedford Colin T CT

Acta crystallographica. Section E, Structure reports online 20080628 Pt 7

IN THE CRYSTAL STRUCTURE OF THE TITLE COMPOUND [SYSTEMATIC NAME: 5H-dibenzo[a,d]cyclo-hepta-triene-5-carboxamide-1,4-dioxane (2/1)], 2C(16)H(13)NO·C(4)H(8)O(2), the cytenamide mol-ecules form a hydrogen-bonded R(2) (2)(8) dimer. The solvent mol-ecule is located between two adjacent cytenamide dimers and forms N-H⋯O hydrogen bonds with one cytenamide mol-ecule from each dimer. ...[more]

PMID: 21202967

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Project description:1,4-Dioxane (1,4-DX) is an environmental contaminant found in drinking water throughout the United States (US). While it is a suspected liver carcinogen, there is no federal or state maximum contaminant level for 1,4-DX in drinking water. Very little is known about the mechanisms by which this chemical elicits liver carcinogenicity. In the present study, we performed chronic and short-term dosing studies in female BDF-1 mice to explore the toxic effects of 1,4-DX. Histopathology studies and a multi-omics approach (transcriptomics and metabolomics) were performed to investigate potential mechanisms of toxicity. Mice were exposed to various concentrations of 1,4-DX (0, 50, 500 and 5,000 mg/L) in their drinking water for one or four weeks. Immunohistochemical analysis of the liver revealed an increase in the number of H2AXγ-positive hepatocytes (a marker of DNA double strand breaks) in mice exposed to 5,000 mg/L 1,4-DX for one and four weeks. In addition, an expansion of precholangiocytes was observed after four weeks of 5,000 mg/L 1,4-DX exposure, as reflected by CK-7 immunostaining. An increase in these markers reflect both DNA damage and repair mechanisms. Liver transcriptomics profiling showed that exposure to 5,000 mg/L 1,4-DX for four weeks resulted in the differential expression of 65 genes compared to controls. Pathway analysis of the transcriptomic data revealed 1,4-DX-induced perturbations in multiple signaling pathways in the liver, including those involved in xenobiotic metabolism, nicotine degradation and glutathione-mediated detoxification. Changes to these pathways as a result of 1,4-DX exposure reflect would be predicted to impact the oxidative stress response, detoxification, and DNA damage. Liver, kidney, stool and urine metabolomics profiling revealed no effect of 5,000 mg/L 1,4-DX exposure for one or four weeks on metabolites. We speculate that this may be reflective of DNA damage being counterbalanced by the repair response, with the net result being a null overall effect on the systemic biochemistry of the exposed mice. Our results show a novel approach for the investigation of environmental chemicals that do not elicit cell death, but have activated the repair systems in response to 1,4-DX exposure

Dataset Information

Cytenamide-1,4-dioxane (2/1).

Publications

Cytenamide-1,4-dioxane (2/1).

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