The protective role of glutathione in chlorothalonil-induced stoxicity to channel catfish


Journal Article

The purpose of this investigation was to examine the nature of the protective role of glutathione (GSH) in liver and gills of channel catfish (Ictalurus punctatus) exposed to chlorothalonil (2,4,5,6 tetrachloroiso-phthalonitrile). In an initial experiment, the acute toxicity of chlorothalonil was enhanced three-fold after channel catfish were depleted of liver and gill GSH by l-buthionine S.R-sulfoximine (BSO. 1000 mg/kg i.p.) and diethyl maleate (DEM, 0.6 ml/kg i.p.), indicating that GSH plays a critical role in mitigating acute chlorothalonil toxicity in this species. In a subsequent experiment, sublethal exposure to chlorothalonil elicited significant increases (p < 0.05) in hepatic GSH concentrations at 72 h and 144 h of exposure. Elevations in hepatic GSH were accompanied by increases in hepatic cysteine concentrations at 72 h and also apparent induction of hepatic gammaglutamylcysteine synthetase (GCS) activity at 144 h. Gill GSH in chlorothalonil-exposed catfish was also significantly increased at 72 h and 144 h. as were increased gill cysteine concentrations. Gill GCS activity was somewhat elevated in chlorothalonil-exposed catfish at 144 h; however, this increase was not statistically significant (p > 0.05). These results indicate that the mechanism of GSH induction in liver and gills of catfish exposed to chlorothalonil involves increased cysteine uptake and also increased GCS activity. The results of this study support the hypothesis that simultaneous exposure to multiple environmental chemicals that utilize or deplete tissue GSH may predis pose fish to acute toxicity. © 1992.

Full Text

Duke Authors

Cited Authors

  • Gallagher, EP; Canada, AT; Di Giulio, RT

Published Date

  • January 1, 1992

Published In

Volume / Issue

  • 23 / 3-4

Start / End Page

  • 155 - 168

International Standard Serial Number (ISSN)

  • 0166-445X

Digital Object Identifier (DOI)

  • 10.1016/0166-445X(92)90049-S

Citation Source

  • Scopus