Published July 10, 2008 | Version v1
Journal article

Proteomic analysis of MCF-7 cells treated with benzo[a]pyrene, dibenzo[a,l]pyrene, coal tar extract, and diesel exhaust extract

  • 1. Department of Zoology, Oregon State University, Corvallis, OR (United States)
  • 2. Department of Environmental and Molecular Biology, Oregon State University, Corvallis, OR (United States)
  • 3. Department of Biochemistry and Biophysics, Oregon State University, Corvallis, OR (United States)

Description

Polycyclic aromatic hydrocarbon (PAH) DNA adducts have been associated with carcinogenesis, which is accompanied by multiple alterations in gene expression. We used two-dimensional electrophoresis to distinguish protein expression changes induced in MCF-7 cells by individual PAH (B[a]P and DB[a,l]P) and PAH mixtures (coal tar extract [SRM 1597] and diesel exhaust extract [SRM 1975]). Spots of interest were identified by MALDI-TOF-TOF. Our results have shown alterations in the expression of heat-shock proteins, cytoskeletal proteins, DNA associated proteins, and glycolytic and mitochondrial proteins. The proteins that were universally altered in expression were actin cytoplasmic 1, tubulin alpha and myosin light chain alkali, cyclophilin B, and heterogeneous ribonucleoprotein B1 (a protein involved in access to telomerase and mRNA maturation). Additional proteins with altered expression include histone H2A.1, heat-shock protein 70-2, galectin-3, nucleoside diphosphate kinase, ATP synthase, and electron transfer flavoprotein. While sharing similarities, each PAH treatment exhibited a unique proteomic fingerprint

Availability note (English)

Available from http://dx.doi.org/10.1016/j.tox.2008.03.019

Additional details

Identifiers

DOI
10.1016/j.tox.2008.03.019;
PII
S0300-483X(08)00138-8;

Publishing Information

Journal Title
Toxicology
Journal Volume
249
Journal Issue
1
Journal Page Range
p. 1-10
ISSN
0300-483X
CODEN
TXCYAC

Optional Information

Copyright
Copyright (c) 2008 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.