Sublethal effects of prolonged exposure to disulfoton in rainbow trout (Oncorhynchus mykiss): cytological alterations in the liver by a potent acetylcholine esterase inhibitor.
Mature male rainbow trout (Oncorhynchus mykiss) were exposed for 28 days to 0, 1, 5, and 20 micrograms/liter disulfoton, i.e., to concentrations well below any macroscopically visible effect due to the primary acute toxic mechanism of acetylcholine esterase inhibition. In an attempt to reveal sublethal injury of disulfoton in rainbow trout, ultrastructural and stereological parameters were recorded in the liver as the central organ of xenobiotic metabolism in fish. Quantitative methods were definitely not able to replace qualitative techniques because, except for mitochondria, peroxisomes, and hepatocellular lipid inclusions, stereological analysis revealed only insignificant variations of hepatocellular components, whereas hepatocytes displayed a complex pattern of numerous delicate qualitative alterations. Effects were most evident within cisternae of the rough endoplasmic reticulum (RER), thus suggesting modifications of protein metabolism. Structural alterations included degenerative effects such as dilation and vesiculation of RER cisternae, formation of concentric RER arrays and augmentation of smooth endoplasmic reticulum, dilation of Golgi cisternae, and the development of cytoplasmic myelinated bodies as well as stacks of membranous material within mitochondria. Structural integrity and augmentation of peroxisomes and mitochondria as well as increased activity of the Golgi system were indicative of adaptive/compensative reactions following disulfoton treatment. In fact, adaptive effects seemed more pronounced than degenerative phenomena resulting in only minor disturbances in hepatocyte structure following disulfoton exposure. Because most effects had to be classified as unspecific responses to environmental or xenobiotic stressors, no distinct mode of sublethal action can be suggested for disulfoton.
Arnold
H
H
Department of Zoology I, University of Heidelberg, Federal Republic of Germany.
Pluta
H J
HJ
Braunbeck
T
T
D000818:Animals; D002800:Cholinesterase Inhibitors / Q000378:metabolism / Q000633:toxicity*; D003593:Cytoplasm / Q000187:drug effects / Q000473:pathology / Q000648:ultrastructure; D004222:Disulfoton / Q000378:metabolism / Q000633:toxicity*; D018870:Endoplasmic Reticulum, Rough / Q000187:drug effects* / Q000473:pathology / Q000648:ultrastructure; D018871:Endoplasmic Reticulum, Smooth / Q000187:drug effects* / Q000473:pathology / Q000648:ultrastructure; D006056:Golgi Apparatus / Q000187:drug effects / Q000473:pathology / Q000648:ultrastructure; D007306:Insecticides / Q000378:metabolism / Q000633:toxicity*; D008099:Liver / Q000187:drug effects* / Q000201:enzymology / Q000293:injuries / Q000648:ultrastructure; D008297:Male; D008854:Microscopy, Electron; D008930:Mitochondria, Liver / Q000187:drug effects / Q000473:pathology / Q000648:ultrastructure; D017686:Oncorhynchus mykiss; D014874:Water Pollutants, Chemical / Q000378:metabolism / Q000633:toxicity
D002800:Cholinesterase Inhibitors; D007306:Insecticides; D014874:Water Pollutants, Chemical; D004222:Disulfoton