Comparative toxicity of organotin compounds to rainbow trout (Oncorhynchus mykiss) yolk sac fry.

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.