Targeting gap junctional intercellular communication by hepatocarcinogenic compounds

J Toxicol Environ Health B Crit Rev. 2020 Aug 17;23(6):255-275. doi: 10.1080/10937404.2020.1781010. Epub 2020 Jun 22.

Abstract

Gap junctions in liver, as in other organs, play a critical role in tissue homeostasis. Inherently, these cellular constituents are major targets for systemic toxicity and diseases, including cancer. This review provides an overview of chemicals that compromise liver gap junctions, in particular biological toxins, organic solvents, pesticides, pharmaceuticals, peroxides, metals and phthalates. The focus in this review is placed upon the mechanistic scenarios that underlie these adverse effects. Further, the potential use of gap junctional activity as an in vitro biomarker to identify non-genotoxic hepatocarcinogenic chemicals is discussed.

Keywords: in vitro; in vivo; Connexin; gap junction intercellular communication; hemichannel; hepatocarcinogenicity; non-genotoxic carcinogenic compounds; risk assessment.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review
  • Video-Audio Media

MeSH terms

  • Animals
  • Cell Communication / drug effects*
  • Connexins / biosynthesis
  • Drug-Related Side Effects and Adverse Reactions
  • Gap Junctions / drug effects*
  • Humans
  • Liver / drug effects*
  • Liver / metabolism
  • Metals / toxicity
  • Peroxides / toxicity
  • Pesticides / toxicity
  • Phthalic Acids / toxicity
  • Risk Assessment
  • Solvents / toxicity
  • Toxins, Biological / toxicity

Substances

  • Connexins
  • Metals
  • Peroxides
  • Pesticides
  • Phthalic Acids
  • Solvents
  • Toxins, Biological
  • phthalic acid