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 da ys to 0, 1, 5, and 20 mu g/liter disulfoton, i.e., to concentrations w ell 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, ultrastructur al and stereological parameters were recorded in the liver as the cent ral 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, st ereological analysis revealed only insignificant variations of hepatoc ellular 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 sugges ting modifications of protein metabolism, Structural alterations inclu ded degenerative effects such as dilation and vesiculation of RER cist ernae, formation of concentric RER arrays and augmentation of smooth e ndoplasmic reticulum, dilation of Golgi cisternae, and the development of cytoplasmic myelinated bodies as well as stacks of membranous mate rial within mitochondria, Structural integrity and augmentation of per oxisomes and mitochondria as well as increased activity of the Golgi s ystem were indicative of adaptive/compensative reactions following dis ulfoton treatment. In fact, adaptive effects seemed more pronounced th an degenerative phenomena resulting in only minor disturbances in hepa tocyte structure following disulfoton exposure, Because most effects h ad to be classified as unspecific responses to environmental or xenobi otic stressors, no distinct mode of sublethal action can be suggested for disulfoton. (C) 1996 Academic Press, Inc.