SIMULTANEOUS EXPOSURE OF FISH TO ENDOSULFAN AND DISULFOTON IN-VIVO - ULTRASTRUCTURAL, STEREOLOGICAL AND BIOCHEMICAL REACTIONS IN HEPATOCYTES OF MALE RAINBOW-TROUT (ONCORHYNCHUS-MYKISS)

The response of male rainbow trout (Oncorhynchus mykiss) liver to combined prolonged exposure to 50 ng/l endosulfan (ES) and 0, 1, 5, or 10 mu g/l disulfoton (DS) was studied using electron microscopical, stereological and biochemical techniques. Both acute and sublethal toxicities of DS increased exponentially by simultaneous exposure to ES. LC,, was determined at 50 ng/l ES plus 20 mu g/l DS. Major sublethal morphological alterations included a 50% increase in cytoplasmic volume due to a 100% increase, dilation and vesiculation of the RER, and a 50% decrease in glycogen deposits. Further reactions were proliferations of mitochondria, myelinated bodies and glycogenosomes, and, at 50 ng/l ES plus 1 mu g/l DS only, a transient increase in the absolute volume of peroxisomes and lysosomes. In terms of liver enzyme activities (mU/g liver), biochemical effects comprised induction of ethoxycoumarin- and ethoxyresorufin-O-deethylases, and of glutathione S-transferase, but depression of esterase, acetylcholine esterase, acid phosphatase, aryl sulfatase, glucose 6-phosphate dehydrogenase, malic enzyme and lactate dehydrogenase, as well as increased lipid peroxidation. In terms of specific enzyme activities (mU/mg protein), there was an increase in uricase, aryl sulfatase, glutathione S-transferase, whereas acetylcholine esterase, malic enzyme and esterase were reduced. No consistent changes were seen in succinate dehydrogenase, catalase, glucose 6-phosphate dehydrogenase, lactate dehydrogenase, and NADPH cytochrome P-45D reductase specific activities. Findings indicate a biphasic reaction to combined ES and DS, with a shift from adaptive to degenerative reactions at 5 mu g/l DS, Acute toxicity of 50 ng/l ES plus 20 mu g/l DS is most likely due to reduced biotransformation capacities by lipid peroxidation-induced membrane damage. Cytochrome P-45D induction and suppression of acetylcholine esterase as typical consequences of ES or DS exposure, respectively, were found as further mechanisms of combined toxicity.