SIMULTANEOUS EXPOSURE OF FISH TO ENDOSULFAN AND DISULFOTON IN-VIVO - ULTRASTRUCTURAL, STEREOLOGICAL AND BIOCHEMICAL REACTIONS IN HEPATOCYTES OF MALE RAINBOW-TROUT (ONCORHYNCHUS-MYKISS)
H. Arnold et al., SIMULTANEOUS EXPOSURE OF FISH TO ENDOSULFAN AND DISULFOTON IN-VIVO - ULTRASTRUCTURAL, STEREOLOGICAL AND BIOCHEMICAL REACTIONS IN HEPATOCYTES OF MALE RAINBOW-TROUT (ONCORHYNCHUS-MYKISS), Aquatic toxicology, 33(1), 1995, pp. 17-43
The response of male rainbow trout (Oncorhynchus mykiss) liver to comb
ined prolonged exposure to 50 ng/l endosulfan (ES) and 0, 1, 5, or 10
mu g/l disulfoton (DS) was studied using electron microscopical, stere
ological and biochemical techniques. Both acute and sublethal toxiciti
es 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 morpho
logical alterations included a 50% increase in cytoplasmic volume due
to a 100% increase, dilation and vesiculation of the RER, and a 50% de
crease 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 lactat
e dehydrogenase, as well as increased lipid peroxidation. In terms of
specific enzyme activities (mU/mg protein), there was an increase in u
ricase, aryl sulfatase, glutathione S-transferase, whereas acetylcholi
ne esterase, malic enzyme and esterase were reduced. No consistent cha
nges were seen in succinate dehydrogenase, catalase, glucose 6-phospha
te dehydrogenase, lactate dehydrogenase, and NADPH cytochrome P-45D re
ductase specific activities. Findings indicate a biphasic reaction to
combined ES and DS, with a shift from adaptive to degenerative reactio
ns at 5 mu g/l DS, Acute toxicity of 50 ng/l ES plus 20 mu g/l DS is m
ost likely due to reduced biotransformation capacities by lipid peroxi
dation-induced membrane damage. Cytochrome P-45D induction and suppres
sion of acetylcholine esterase as typical consequences of ES or DS exp
osure, respectively, were found as further mechanisms of combined toxi
city.