Toxicological Effects Of Benzo(a) Pyrene, Tributyltin And Their Mixture To Sebastiscus Marmoratus

Marine fish Sebastiscus marmoratus was adopted as experimental animal. Toxicological effects were studied on two kinds of typical organic contaminants in marine environments, Polycyclic aromatic hydrocarbons (PAHs) and organotins. Sebastiscus marmoratus exposed to BaP (10, 100,1000 ng/L), TBT (1, 10, 100 ng/L) and their mixture (5 ng/L BaP+0.5 ng/L TBT, 50 ng/L BaP+5 ng/L TBT, 500 ng/L BaP+50 ng/L TBT) were randomly sampled after exposure for 0, 7, 25, 50 days and transferred to clean water to recover for 7 and 20 days, respectively. The physiological, biochemical and molecular parameters were analyzed to assess the effects of BaP, TBT and their mixture to metabolism, hepatic detoxification enzyme system, antioxidant system and DNA damage. Furthermore, the availability of these biomarkers to monitor marine pollution by BaP, TBT and their mixture were assessed. The main results as follows:1. Levels of BaP metabolites in the bile were increased in a dose-dependent manner in the fish exposed through water to BaP, and reflected contamination gradients of PAHs. However, EROD and GST activities should be taken into account to assess time-effect relation. Total biliary Sn²⁺ content in fish is feasible to serve as an indicator to monitor severe organotin pollution, and as far as combined effects are concerned, BaP increased the excretion of TBT to bile.2. Environmentally relevant concentrations of BaP and TBT influenced hepatic detoxification enzyme system significantly. CYPIA level inceased in harmony with BaP concentration with Western blot analysis, so CYPIA level is feasible to serve as a good biomarker to monitor PAHs pollution. EROD and ECOD are both phase I enzymes. There were complicated relations of time-effect and dose-effect between EROD activity and exposure of BaP, TBT or their mixture. Antagonistic interactions occurred after 25 days exposure to the mixure of BaP and TBT. It is fuzzy to merely use EROD activity as biomarker to assess PAHs or TBT pollution. Therefore, it is vital to assemble CYPIA level or BaP-type metabolites to assess PAHs pollution and integrate other biomarkers (e.g. total biliary Sn²⁺content) to assess TBT pollution in marine environment. ECOD activity was induced by BaP, TBT or their mixture at high concentrations after 50 days exposure, and it is advisable to use ECOD activity as a biomarker to assess severe PAHs or TBT pollution. UDPGT was analyzed as phase II enzyme. There were scarcely significant effects of BaP, TBT or their mixture to UDPGT activity after 25 d exposure.3. Combined effects of BaP and TBT to antioxidant system were complicated, and antagonistic interactions were dominating. SOD, GST activities were induced and GSH content were increased after 50 days exposure to BaP, and it is feasible to integrate them into PAHs pollution monitoring program. MDA content was increased and SOD, GPx activities were induced, and GSH content was decreased after 50 days exposure to TBT, so it is feasible to integrate them into TBT pollution monitoring program. In the same way, MDA content was increased and GST, GPx activities were induced after 50 days exposure to the mixture of BaP and TBT, so it is feasible to integrate them into PAHs with the addition of TBT pollution monitoring program in marine environment.4. DNA single strand break damage was aggravated along with the increase of exposure concentration and the elongation of exposure time, so DNA single strand break damage is feasible to serve as a potential biomarker to monitor the pollution of PAHs, TBT or their mixture, because good relations of time-effect and dose-effect existed. As far as the results after 25 days and 50 days exposure are concerned, combination of BaP and TBT alleviated the degree of DNA damage which was consistent with the inhibition of BaP metabolism by TBT and the promotion of TBT excretion by BaP.Based on the results we obtained, we conclude that combined toxicological effects of BaP and TBT at environmentally relevant concentrations were complicated, and antagonistic interactions were dominating. TBT inhibited BaP metabolism, and BaP facilitated TBT metabolism and excretion.