Correlations of Gut Microbial Community Shift with Hepatic Damage and Growth Inhibition of Carassius auratus Induced by Pentachlorophenol Exposure

Environ Sci Technol. 2015 Oct 6;49(19):11894-902. doi: 10.1021/acs.est.5b02990. Epub 2015 Sep 28.

Abstract

Goldfish (Carassius auratus) were exposed to 0-100 μg/L pentachlorophenol (PCP) for 28 days to investigate the correlations of fish gut microbial community shift with the induced toxicological effects. PCP exposure caused accumulation of PCP in the fish intestinal tract in a time- and dose-dependent manner, while hepatic PCP reached the maximal level after a 21 day exposure. Under the relatively higher PCP stress, the fish body weight and liver weight were reduced and hepatic CAT and SOD activities were inhibited, demonstrating negative correlations with the PCP levels in liver and gut content (R < -0.5 and P < 0.05 each). Pyrosequencing of the 16S rRNA gene indicated that PCP exposure increased the abundance of Bacteroidetes in the fish gut. Within the Bacteroidetes phylum, the Bacteroides genus had the highest abundance, which was significantly correlated with PCP exposure dosage and duration (R > 0.5 and P < 0.05 each). Bioinformatic analysis revealed that Bacteroides showed quantitatively negative correlations with Chryseobacterium, Microbacterium, Arthrobacter, and Legionella in the fish gut, and the Bacteroidetes abundance, Bacteroides abundance, and Firmicutes/Bacteroidetes ratio played crucial roles in the reduction of body weight and liver weight under PCP stress. The results may extend our knowledge regarding the roles of gut microbiota in ecotoxicology.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Bacteroidetes / drug effects
  • Bacteroidetes / genetics
  • Catalase / metabolism
  • Environmental Exposure / analysis*
  • Gastrointestinal Microbiome / drug effects*
  • Gastrointestinal Tract / drug effects
  • Gastrointestinal Tract / metabolism
  • Goldfish / growth & development*
  • Goldfish / microbiology*
  • Liver / drug effects*
  • Liver / pathology
  • Oxidative Stress / drug effects
  • Pentachlorophenol / toxicity*
  • Principal Component Analysis
  • RNA, Ribosomal, 16S / genetics
  • Superoxide Dismutase / metabolism

Substances

  • RNA, Ribosomal, 16S
  • Pentachlorophenol
  • Catalase
  • Superoxide Dismutase