GLUTATHIONE-DEPENDENT DEFENSE IN CHANNEL CATFISH (ICTALURUS-PUNCTATUS) AND BROWN BULLHEAD (AMERIURUS-NEBULOSUS)

Glutathione-dependent defense against xenobiotic toxicity is a multifa ceted phenomenon that has been well characterized in mammals. This stu dy undertakes a comparison of two benthic fish species, the channel ca tfish and brown bullhead, in terms of characteristics of the glutathio ne system. The channel catfish, a species that has seldom been observe d to express pollutant-mediated neoplasia in field studies, was observ ed to have significantly higher constitutive levels of hepatic total g lutathione and reduced glutathione (GSH). Brown bullhead, a species th at is often observed to express neoplasia in contaminated systems, had significantly higher hepatic levels of glutathione disulfide. Further more, catfish expressed higher levels of activity of the enzymes gamma -glutamylcysteine synthetase (GCS), glutathione reductase (GR), and gl utathione S-transferase, whereas bullhead expressed higher hepatic glu tathione peroxidase (GPOX) activity. Both species responded to treatme nt with the redox active quinone, menadione, by expressing elevated he patic content of total glutathione. However, the induction response wa s more rapid and more extensive in catfish compared to that in bullhea d. This is attributable to the observed interspecific difference in GC S activity. Following treatment with the organic peroxide, tert-butyl hydroperoxide (t-BOOH), bullhead hepatic glutathione was depleted up t o 4 hr post-treatment, whereas catfish demonstrated no significant dep letion of glutathione in response to t-BOOH. The differing responses t o t-BOOH are attributable to interspecific differences in hepatic GPOX and GR activity. Bullhead, therefore, appear to be more susceptible t o the effects of GSH arylators and oxidants based upon constitutive le vels of glutathione, related enzyme activities, and the response of th is system to model xenobiotics. The role of glutathione-dependent defe nse systems in determining species susceptibility to endpoints of xeno biotic toxicity, such as neoplasia, is discussed. (C) 1994 Academic Pr ess, Inc.