Induction of liver GST transcriptions by tert-butylhydroquinone reduced microcystin-LR accumulation in Nile tilapia (Oreochromis niloticus)

Ecotoxicol Environ Saf. 2013 Apr:90:128-35. doi: 10.1016/j.ecoenv.2012.12.021. Epub 2013 Jan 24.

Abstract

The cyanobacterial toxin, MC-LR, is predominantly presented during toxic cyanobacterial blooms and is consumed by phytoplanktivorous fish and zooplanktivorous fish directly. Detoxification of MC-LR in liver was believed to begin with conjugate formation with GSH, catalyzed by GSTs. MC-LR GSH conjugates display increased solubility and are subjected to accelerated biliary excretion. In this study, we showed that the mRNA transcriptions of GSTA, GPX and UCP2 were increased within 8h following MC-LR exposure in isolated hepatocytes of Nile tilapia, confirming the roles of phase II enzymes, especially GSTs, in MC-LR detoxification in tilapia. The widely used food-additive, synthetic antioxidant, tert-butylhydroquinone (tBHQ) has been shown to induce phase II enzymes including GSTs, via the antioxidant responsive elements (ARE) locate in the regulatory regions of these genes. Our results also showed that the transcription of various GSTs, including GSTA, GSTR2 and GSTT were significantly induced by tBHQ in Nile tilapia. In consistence, fish fed on tBHQ-containing diet (0.01 percent tBHQ) showed significantly reduced MC-LR accumulation in liver tissues 48 h after an oral administration of a single dose of 250 μg MC-LR/kg body weight (bwt). The findings in this research suggested that tBHQ could reduce MC-LR accumulations in liver, likely through the induction of phase II metabolizing enzymes such as GSTs. Subacute effects of tBHQ and its potential applications in fishery need to be further investigated.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Caenorhabditis elegans Proteins
  • Cichlids / genetics
  • Cichlids / metabolism
  • Cichlids / physiology*
  • Enzymes / genetics
  • Fishes / metabolism
  • Gene Expression Regulation, Enzymologic / drug effects*
  • Glutathione Transferase / genetics*
  • Hydroquinones / toxicity*
  • Inactivation, Metabolic
  • Liver / drug effects*
  • Liver / enzymology
  • Liver / metabolism
  • Microcystins / metabolism*
  • Transcription Factors

Substances

  • Caenorhabditis elegans Proteins
  • DIE-1 protein, C elegans
  • Enzymes
  • Hydroquinones
  • Microcystins
  • Transcription Factors
  • 2-tert-butylhydroquinone
  • Glutathione Transferase