Acute Toxicity And Bioaccumulation Of Tributyltin In Tissues Of Urolophus jamaicensis (Yellow Stingray)
Titel:
Acute Toxicity And Bioaccumulation Of Tributyltin In Tissues Of Urolophus jamaicensis (Yellow Stingray)
Auteur:
Dwivedi, J. Trombetta, L. D.
Verschenen in:
Journal of toxicology and environmental health. Part A
Paginering:
Jaargang 69 (2006) nr. 14 pagina's 1311-1323
Jaar:
2006-08-01
Inhoud:
Tributyltin oxide (TBTO) is the main constituent of tin-based antifouling marine paint used on the hulls of ships to prevent the growth of fouling organisms. TBTO was shown to be hazardous to nontarget organisms. The stingray, Urolophus jamaicensis, may represent the ideal study organism for the adverse effects of TBTO to elasmobranches. This study investigated the toxicity and accumulation of tin in the gill tissue of the stingray U. jamaicensis after acute exposure to TBTO. This work demonstrates the alterations in the morphological architecture of the gill using electron and light microscopy, the induction of stress proteins, and peroxidative damage in response to tributyltin (TBT) exposure. A captured population of U. jamaicencis was housed in isolated, static tank systems. After a minimum 30-d acclimation period, the animals were exposed to one of 5 experimental doses of TBTO (4 μg/L, 2 μg/L, 1 μg/L, 0.5 μg/L, or 0.05 μg/L). A sixth group served as a control population. At 3h following treatment, animals were sacrificed and gill tissue was extracted, processed, and stored for analysis. Results indicate that U. jamaicensis is hypersensitive to TBT exposure. The elasmobranch gill showed a distorted, swollen epithelium with exfoliation following acute exposure to as little as 0.05 μg/L TBTO for 3 h. Graphite furnace atomic absorption spectroscopy (GFAAS) results indicate that tissues of treated animals contained a significantly increased tin concentration as compared to controls. Western blot analysis demonstrated the induction of the stress proteins Hsp 70 and HO1. 4-Hydroxynonenol (4HNE) adduct formation determined by Western blot analysis provides further evidence that observed membrane degradation is a result of lipid peroxidation.
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