GLUTATHIONE-DEPENDENT DETOXIFYING ENZYMES IN RAINBOW-TROUT LIVER - SEARCH FOR SPECIFIC BIOCHEMICAL MARKERS OF CHEMICAL STRESS

Activities of trout liver microsomal glutathione S-transferase (GST) a nd a series of cytosolic glutathione-dependent detoxifying enzymes wer e determined after a single intraperitoneal treatment with phenobarbit al, 2,2-bis (p-chlorophenyl)-1,1-dichloroethane (p,p'-DDE), 2,3,-dimet hoxynaphthoquinone (NQ), or 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) . This study aimed to find xenobiotic-specific parameters applicable a s biochemical markers of the impacts of the prototypal xenobiotics. Th e effects of xenobiotics on cytosolic GST activities were substrate de pendent. The rate of conjugation of p-nitrobenzyl chloride was signifi cantly induced by higher doses of p,p'-DDE or NQ. The conjugation of e thacrynic acid was enhanced by phenobarbital, p,p'-DDE, and NQ (i.e., by xenobiotics that do not induce cytochrome P4501A forms). The GST ac tivity against 1,2-epoxy-3-(p-nitrophenoxy)propane was induced only by phenobarbital and by lower doses of p,p'-DDE. The cytosolic GST activ ity, measured with 1-chloro-2,4-dinitrobenzene as a substrate, was onl y weakly increased by phenobarbital, TCDD, higher doses of p,p'-DDE, o r by NQ at the lowest dose of 1 mg/kg. Although the latter activity is frequently used as a biomarker in ecotoxicology, various factors (inc luding its weak inducibility) indicate that this biochemical parameter is probably not a suitable indicator of contamination in fish. Simila rly, cytosolic glutathione peroxidase was not affected by the prototyp al xenobiotics and appeared to be an unsuitable bioindicator of oxidat ive impacts of the tested compounds. On the other hand, microsomal GST activity was nonspecifically increased by phenobarbital, NQ, TCDD, an d high doses of p,p'-DDE. Glutathione reductase, another potential bio marker of oxidative stress, was induced by phenobarbital, NQ, and, to a lesser extent, p,p'-DDE; therefore it appeared to be a less sensitiv e indicator to the exposure to prototypal xenobiotics than the microso mal GST. We conclude that the increase of microsomal GST and cytosolic glutathione reductase activities could become useful biochemical mark ers of oxidative stress, while the induction of cytosolic GST activiti es toward ethacrynic acid and probably also toward p-nitrobenzyl chlor ide appear to hold promise as biochemical markers of specific impacts of p,p'-DDE and redox cycling quinones in trout liver.