de Vries H, Penninks A H, Snoeij N J, Seinen W
Department of Veterinary Pharmacology, Pharmacy and Toxicology, University of Utrecht, Netherlands.
Sci Total Environ. 1991 Apr 15;103(2-3):229-43. doi: 10.1016/0048-9697(91)90148-8.
The comparative toxicity of various organotin compounds was investigated in early life stages of the rainbow trout. Beginning with yolk sac fry, trout were continuously exposed for 110 days to tributyl- (TBTC), triphenyl- (TPhTC) or tricyclohexyltin chloride (TCHTC) at concentrations of 0.12-15 nM, to trimethyltin chloride (TMTC) at concentrations of 3-75 nM or to dibutyl- (DBTC) or diphenyltin chloride (DPhTC) at 160-4000 nM. The diorganotin compounds DBTC and DPhTC were about three orders of magnitude less toxic than the triorganotin homologs TBTC and TPhTC. Both for DBTC and DPhTC, a no-observable-effect concentration (NOEC) of 160 nM was established, corresponding to 40 and 60 ppb, respectively. Of the triorganotin compounds, TCHTC appeared to be the most toxic, inducing 100% mortality within 1 week at a concentration of 3 nM. Only a few trout survived exposure to 0.6 nM TCHTC for 110 days. TBTC and TPhTC caused acute mortality at a concentration of 15 nM. For both TBTC and TPhTC a NOEC of 0.12 nM was established, corresponding to water concentrations of 40 and 50 ppt, respectively. Histopathological examination revealed depletion of glycogen in liver cells of both di- and triorganotin exposed fish, except in the case of TMTC. No signs of toxicity were observed in fish exposed to up to 75 nM TMTC, the highest concentration tested. Atrophy of the thymus, the most prominent sign of toxicity of di- and tributyltin compounds in mammalian species, was not observed in early life stages of rainbow trout. Tail melanization was observed in the groups exposed to 3 nM TPhTC, 3 nM TBTC, 800 nM DBTC and 800 nM DPhTC. At the end of the exposure period, resistance to infection was examined by an intraperitoneal challenge with Aeromonas hydrophila, a secondary pathogenic bacterium to fish. Resistance of bacterial challenge was found to be decreased even at the lowest-effect concentration of both di- and triorganotin compounds.
研究了各种有机锡化合物对虹鳟鱼幼鱼期的相对毒性。从卵黄囊仔鱼开始，虹鳟鱼连续110天暴露于浓度为0.12 - 15 nM的三丁基氯化锡（TBTC）、三苯基氯化锡（TPhTC）或三环己基氯化锡（TCHTC），浓度为3 - 75 nM的三甲基氯化锡（TMTC），或浓度为160 - 4000 nM的二丁基氯化锡（DBTC）或二苯基氯化锡（DPhTC）。二有机锡化合物DBTC和DPhTC的毒性比三有机锡同系物TBTC和TPhTC低约三个数量级。对于DBTC和DPhTC，均确定了160 nM的无可见效应浓度（NOEC），分别对应于40和60 ppb。在三有机锡化合物中，TCHTC似乎毒性最大，在浓度为3 nM时1周内导致100%死亡。只有少数虹鳟鱼在暴露于0.6 nM TCHTC 110天后存活。TBTC和TPhTC在浓度为15 nM时导致急性死亡。对于TBTC和TPhTC，均确定了0.12 nM的NOEC，分别对应于水浓度40和50 ppt。组织病理学检查显示，除TMTC外，暴露于二有机锡和三有机锡的鱼肝细胞中的糖原均减少。在暴露于高达75 nM TMTC（测试的最高浓度）的鱼中未观察到毒性迹象。在虹鳟鱼幼鱼期未观察到胸腺萎缩，而胸腺萎缩是二丁基锡和三丁基锡化合物在哺乳动物物种中最显著的毒性迹象。在暴露于3 nM TPhTC、3 nM TBTC、800 nM DBTC和800 nM DPhTC的组中观察到尾部黑化。在暴露期结束时，通过腹腔注射嗜水气单胞菌（一种鱼类继发性病原菌）来检测抗感染能力。发现即使在二有机锡和三有机锡化合物的最低效应浓度下，细菌攻击的抵抗力也会降低。
