Oxidative stress and liver toxicity in rats and human hepatoma cell line induced by pentachlorophenol and its major metabolite tetrachlorohydroquinone

Ying J. Wang, Ching Chang Lee, Wen Ching Chang, Hung B. Liou, Yuan Soon Ho

Research output: Contribution to journalArticle

62 Citations (Scopus)

Abstract

Pentachlorophenol (PCP) is a pesticide used worldwide in industrial and domestic applications. It is used extensively as biocide and wood preservatives. Metabolic studies carried out in rodents and human liver homogenates have indicated that PCP undergoes oxidative dechlorination to form tetrachlorohydroquinone (TCHQ). Free radical catalyzed tissue injury is thought to play a fundamental role in human disease. In the present study, we examined the effects of PCP and TCHQ on the induction of lipid peroxidation and liver injury in rats. In addition, the cytotoxic dose, cell death mechanisms and related gene expressions induced by PCP and TCHQ were also determined for human hepatoma cell line (Hep G2). The results indicated that more toxic effects could be observed both in rats and human hepatoma cell line treated with TCHQ than its parent compound, PCP. Oxygen species may be involved in the mechanism of TCHQ intoxication since the urinary 8-epi-PGF2α and AST, ALT activities can be induced by TCHQ and attenuated by vitamin E treatment. Apoptosis features were found in cells treated with TCHQ but not PCP. TCHQ-induced cell damage may issue signals for the induction of HSPs, the decrease of the bcl/bax protein ratio and the decrease of CAS gene, whereas the PCP-induced damage may not.

Original languageEnglish
Pages (from-to)157-169
Number of pages13
JournalToxicology Letters
Volume122
Issue number2
DOIs
Publication statusPublished - Jun 20 2001

Keywords

  • Cell death mechanisms
  • Gene expressions
  • Lipid peroxidation
  • Liver injury
  • Pentachlorophenol
  • Tetrachlorohydroquinone

ASJC Scopus subject areas

  • Toxicology

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