科研之友
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摘要
Several studies have shown that fluorotelomer-based compounds can be metabolized to poly- and perfluorinated carboxylates, such as perfluorooctanoate (PFOA). Research has predominately focused on the 8:2 fluorotelomer alcohol (8:2 FTOH), however, the biotransformation pathway is not well understood. Specifically, there is uncertainty regarding the biological fate of the 8:2 fluorotelomer unsaturated carboxylate (FTUCA) and 7:3 fluorotelomer saturated carboxylate (FTCA). The objective of this study was to further elucidate the pathway for 8:2 FTOH biotransformation through dosing rainbow trout with three 8:2 FTOH metabolism intermediates: the 7:3 FTCA (CF(3)(CF(2))(6)CH(2)CH(2)C00(-1)), 8:2 FTCA (CF(3)(CF(2))(7)CH(2)COO(-)), and 8:2 FTUCA (CF(3)(CF(2))(6)CF=CHCOO(-)). This study represents the first investigation of these three labile intermediate metabolites in an in vivo system. The parent compounds were dosed via the diet and the parent compounds and intermediates were monitored in the blood and liver during the 7-day uptake phase and 10-day elimination phase. Exposure to the 7:3 FTCA did not result in the formation and accumulation of PFOA, but resulted in low levels of the 7:3 FUCA and perfluoroheptanoate, a novel finding. PFOA was formed in the 8:2 FTUCA and 8:2 FTUCA dosing. In addition, the 7:3 FTCA was formed during exposure to both the 8:2 FTCA and 8:2 FTUCA. Elimination half-lives were 5.1 d (95% confidence interval: 3.1-14 d) for 7:3 FTCA, 1.2 d (1.1-1.3 d) for 8:2 FTCA, and 0.39 d (0.31-0.53 d) for 8:2 FTUCA. The observed differences in the elimination half-life may be the result of differences in either the depuration or metabolism rate. Based on the findings of this study, and reported analogous literature pathways, we proposed a "beta-like-oxidation" pathway for PFOA formation proceeding from the 8:2 FTUCA > 7:3 beta-keto acid > 7:2 ketone > PFOA. Alternatively PFOA could be formed directly through the beta-oxidation of the 7:3 beta-keto acid.
- 出版日期2010-7-1
