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Spherical silica nanoparticles promote malignant transformation of BEAS-2B cells by stromal cell-derived factor-1α (SDF-1α).
J Int Med Res
March 2019
1 Department of Laboratory Medicine, First Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, China.
Objective: This study aimed to examine the role of spherical silica nanoparticles (SiNPs) on human bronchial epithelial (BEAS-2B) cells through inflammation.
Methods: Human mononuclear (THP-1) cells and BEAS-2B cells were co-cultured in transwell chambers and treated with 800 mmol/L benzo[ a]pyrene-7, 8-dihydrodiol-9, 10-epoxide (BPDE) and 12.5 µg/mL SiNPs for 24 hours.
Comparative Tumorigenicity and DNA Damage Induced by Dibenzo[ def,p]chrysene and Its Metabolites in the Mouse Ovary.
Chem Res Toxicol
November 2018
Charles River Laboratories-Contractor Supporting: National Institute of Allergy and Infectious Diseases, Frederick , Maryland 21702 , United States.
Ovarian cancer ranked second in incidence among gynecologic cancers, but it causes more deaths than any other gynecologic cancer; at present there is no curative treatment beyond surgery. Animal models that employ carcinogens found in the human environment can provide a realistic platform to understand the mechanistic basis for disease development and to design rational chemopreventive/therapeutic strategies. We and others have shown that the administration of the environmental pollutant and tobacco smoke constituent dibenzo[ def,p]chrysene (DBP) to mice by several routes of exposure can induce tumors in multiple sites including the ovary.
View Article and Find Full Text PDFCytochrome P450 1b1 in polycyclic aromatic hydrocarbon (PAH)-induced skin carcinogenesis: Tumorigenicity of individual PAHs and coal-tar extract, DNA adduction and expression of select genes in the Cyp1b1 knockout mouse.
Toxicol Appl Pharmacol
September 2015
Department of Environmental and Molecular Toxicology, Oregon State University, Corvallis, OR 97331, USA; Superfund Research Center, Oregon State University, Corvallis, OR 97331, USA; Environmental Health Sciences Center, Oregon State University, Corvallis, OR 97331, USA.
Article Synopsis
- FVB/N mice with varying expressions of Cyp 1b1 were studied for their response to different carcinogens in a two-stage skin tumor experiment, focusing on DBC, BaP, and CTE.
- The Cyp 1b1 null mice showed reduced tumor incidence and progression when initiated with DBC but not with BaP or CTE.
- Gene expression analysis indicated that the absence of Cyp 1b1 led to decreased levels of certain protective genes and a trend of reduced DNA adducts related to DBC, highlighting its critical role in DBC-induced skin carcinogenesis.
Mutagenicity and tumorigenicity of the four enantiopure bay-region 3,4-diol-1,2-epoxide isomers of dibenz[a,h]anthracene.
Carcinogenesis
September 2013
Susan Lehman Cullman Laboratory for Cancer Research, Department of Chemical Biology, Ernest Mario School of Pharmacy, Rutgers, The State University of New Jersey, 164 Frelinghuysen Road, Piscataway, NJ 08854, USA.
Article Synopsis
- The study examined the mutagenic activity of two enantiomers of bay-region dibenz[a,h]anthracene diol epoxides, focusing on their configurations (cis and trans) and how they influence mutagenesis in Salmonella and Chinese hamster cells.
- The (1S,2R,3S,4R) isomer showed the highest mutagenic activity in Salmonella strains, while the (1R,2S,3S,4R) isomer was the most active in the Chinese hamster cells and also proved to be a strong tumor initiator in mouse models.
- Overall, the research underscores that certain stereochemical configurations, particularly the [R,S,S,R] configuration, are
Regulation of benzo[a]pyrene-mediated DNA- and glutathione-adduct formation by 2,3,7,8-tetrachlorodibenzo-p-dioxin in human lung cells.
Chem Res Toxicol
January 2011
Center for Cancer Pharmacology, University of Pennsylvania, Philadelphia, Pennsylvania 19104-6610, USA.
Environmental carcinogens, such as polycyclic aromatic hydrocarbons (PAHs), require metabolic activation to DNA-reactive metabolites in order to exert their tumorigenic effects. Benzo[a]pyrene (B[a]P), a prototypic PAH, is metabolized by cytochrome P450 (P450) 1A1/1B1 and epoxide hydrolase to (-)-B[a]P-7,8-dihydro-7,8-diol (B[a]P-7,8-dihydrodiol). B[a]P-7,8-dihydrodiol then undergoes further P4501A1/1B1-mediated metabolism to the ultimate carcinogen, (+)-anti-7,8-dihydroxy-9,10-epoxy-7,8,9,10-tetrahydro-B[a]P (B[a]PDE), which forms DNA-adducts primarily with 2'-deoxyguanosine (dGuo) to form (+)-anti-trans-B[a]PDE-N(2)-dGuo (B[a]PDE-dGuo) in DNA.
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