Abstract
The acute toxicity of tributyltin oxide (TBTO) was determined in larvae (nauplii, zoeae 1–3, mysis 1–3), post-larvae (PL stages) and juvenile shrimp (Penaeus japonicus Bate), in two media, seawater (SW) and diluted seawater (DSW; 1100 and 550 mosm kg−1 ≈37 and 19‰). Survival, osmoregulatory capacity and Na+-K+ ATPase activity were measured. A gill and epipodite histopathological study was also conducted. The 24 and 48 h LC50s values for TBTO in SW ranged from 2.03 μg l−1 (1.7–2.4) and 0.88 μg l−1 (0.8–1.0) for nauplii to 773 μg l−1 (344–1823) and 708 μg l−1 (361–1608) for juveniles. The 96 h LC50s values in SW ranged from 19.4 μg l−1 (12.6–27.3) for PL5 to 370 μg l−1 (202–662) for juveniles. The 96 h LC50 value was not affected by salinity in juveniles. Tolerance to TBTO tended therefore to increase with the development from larval to juvenile instars. In juveniles kept in SW and in DSW, acute TBTO-exposures decreased the osmoregulatory capacity (OC=difference between the hemolymph osmolality and the osmolality of the medium) of animals exposed to lethal and sublethal concentrations. Effects of TBTO exposure on hypo- and hyper-OC were time- and dose-dependent and the ability to osmoregulate was recovered after exposure of the shrimp to water free of TBTO for 48–120 h. These experiments confirmed OC as a valuable tool for monitoring the physiological state of peneid shrimp. Gill and epipodite Na+-K+ ATPase activities were not altered in SW and DSW after acute TBTO-exposures, either at sublethal or at lethal concentrations. Haemocytic congestion (thrombosis), multiple necrosis and nephrocyte hyperplasia were observed in gill lamellae of exposed shrimp. Multiple necrosis and lacunae in the epithelial monolayers were also observed in epipodites. At lethal concentrations, the interconnecting lacunae were reduced and/or replaced by proliferating tissues. Epithelial cells were peeling and oedema was observed. For both tissues, histopathological effects increased with the dose and they are probably the cause of impaired osmoregulation.
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