| Summary: | The exposure of humans and wildhfe to exogenous chemicals is increasing annually, and it has been recognised for many years that some of these chemicals may be capable of disrupting the endocrine system, and causing detrimental effects. However little is known about the mechanisms behind these processes. Many endocrine disrupting chemicals (EDC's) are reactive chemicals that exhibit multiple mechanisms of toxicity by acting at different sites within the body and there is increasing evidence to suggest that many of them have carcinogenic, mutagenic, immunotoxic, or neurotoxic potential (Choi et al., 2004). Tributyltin is one of best known EDC's and evidence is accumulating to suggest that this compound is genotoxic. It is unclear how this compound causes genetic toxicity. It was previously unclear whether the toxicity seen was caused directly by the compound itself, or by increasing the testosterone titres in exposed organisms. Evidence suggested that increased testosterone titres were the major cause of genetic damage (Tillmann et al., 2001). This study shows that all damage cannot be attributed to testosterone alone, and that TBT is capable of causing genetic toxicity by some other mechanism. To prove this, adult dog-whelks (Nucella lapillus) were exposed to testosterone, and TBT, with and without the presence of an androgen blocker, cyproterone acetate (CPA). Results showed a significant decrease in genetic damage with the inclusion of CPA in the testosterone exposures, but the extent of damage reduction was not seen when CPA was added to the TBT exposures. This shows that testosterone cannot be solely responsible for all the genetic damage seen in TBT exposed dog-whelks. A possible alternative mechanism by which TBT may be genotoxic is through the induction of endonucleases via disruption of intracellular calcium homeostasis (Orrenius et al., 1992). Faculty of Science
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