Alterations to proteome and tissue recovery responses in fish liver caused by a short-term combination treatment with cadmium and benzo[a]pyrene

Pedro M. Costa, Eduardo Chicano-Gálvez, J. López-Barea,, Tomás Ángel DelValls, Maria Helena Ferrão Ribeiro da Costa

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39 Citations (Scopus)

Abstract

The livers of soles (Solea senegalensis) injected with subacute doses of cadmium (Cd), benzo[a]pyrene (NW), or their combination, were screened for alterations to cytosolic protein expression patterns, complemented by cytological and histological analyses. Cadmium and B[a]P, but not combined, induced hepatocyte apoptosis and Kupfer cell hyperplasia. Proteomics, however, suggested that apoptosis was triggered through distinct pathways. Cadmium and B[a]P) caused upregulation of different anti-oxidative enzymes (peroxiredoxin and glutathione peroxidase, respectively) although co-exposure impaired induction. Similarly, apoptosis was inhibited by co-exposure, to which may have contributed a synergistic upregulation of tissue metalloproteinase inhibitor, beta-actin and a lipid transport protein. The regulation factors of nine out of eleven identified proteins of different types revealed antagonistic or synergistic effects between Cd and B[all) at the prospected doses after 24 h of exposure. The results indicate that co-exposure to Cd and B[a]P may enhance toxicity by impairing specific responses and not through cumulative damage. (C) 2010 Elsevier Ltd. All rights reserved.
Original languageEnglish
Pages (from-to)3338-3346
JournalEnvironmental Pollution
Volume158
Issue number10
DOIs
Publication statusPublished - Oct 2010

Keywords

  • Apoptosis
  • Hepatic parenchyma
  • Metal
  • Polycyclic aromatic hydrocarbon
  • Proteomics

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