| Tris-(2,3-dibromopropyl) isocyanurate (TBC) is a heterocyclic brominated flame retardant that was recently detected in the environment, TBC is semi-volatile and can accumulate in the lipid of some species, but little is known about its effect on aquatic organisms. In this paper, zebrafish were exposed to single TBC and co-exposed to TBC and 17β-estradiol (E2) to detect the toxicity effects of TBC to adult zebrafish and its possible toxic mechanism to zebrafish and ecosystems.We exposed adult zebrafish to 0,0.25,1 and 4 mg/L TBC for 28 d and measured the effect on survival, growth, histopathology, hormone levels, enzyme activity, and gene expression. TBC exposure had no effect on survival or growth. We observed significant damage to the liver and gill, including hepatocellular swelling and fatty degeneration in the liver as well as proliferation and edema of epithelial cells in the gills. In addition, exposure to 4 mg/L TBC induced proliferation of goblet cells in the intestine of both sexes, acellular areas in the testis, and thinly scattered vitellogenic granules in vitellogenic oocytes. TBC exposure had no effect on the levels of thyroid hormones, testosterone, estradiol, liver superoxide dismutase activity, malondialdehyde content, and brain cholinesterase activity. By contrast, hepatic vitellogenin and cytochrome P4501A gene expression was significantly down-regulated in both male and female zebrafish in response to TBC exposure.Adult male zebrafish were exposed to TBC and 17β-estradiol (E2) to evaluate the potential toxic mechanism of TBC. We found that TBC could significantly inhibit the raise of condition factor and could also alleviate the low proportion of spermatids and the development retardant of the sex gland, which were induced by E2. The exposure of E2 led to fatty degeneration of the hepatocy te, an increase in MDA content and steadiness of SOD activity, whereas the co-exposure of TBC and E2 could alleviate the MDA enhancement, while the hepatocytic fatty degeneration and the SOD activity remained unchanged. Moreover, TBC could significantly suppress the increased expression of vitellogenin (VTG) which was induced by E2. These results suggest that TBC could cause obvious endocrine disruption. Therefore, it is needed to characterize the toxicity of heterocyclic brominated flame retardant (BFRs), such as TBC, as they may cause potential contamination to aquatic ecosystems.In order to investigate the reproductive effects of TBC, Fo adult female zebrafish were exposed to TBC for 14d and then renewed in TBC-free system water for another 24d, so as Results showed that TBC inhibited the spawn ability of zebrafish (Fo). As for the offspring (F1), TBC caused the decrease its hatching rate, induced defects in gas bladder of zebrafish larvae as well as diminished the areas of gas bladder. This toxic effects were weaken with the expanding of renew time indicating that transfer from matrix to offspring is one of the main metabolic pathways of TBC. In addition, after the renewed in TBC-free system water, the SOD activity in brain of fish in control group was significantly change. However, the SOD activity in brain of TBC-treated fish was stand sill which suggested that TBC might inhibit the environment stress ability of zebrafish, we deduced that TBC might cause irreversible toxic effects to brain of zebrafish.In a word, TBC exposure caused significantly down-regulated expression of hepatic vitellogenin gene in both male and female zebrafish; TBC could significantly suppress the increased expression of vitellogenin (VTG) which was induced by E2. Combine with our finding that TBC exposure cause dramatic injury in zebrafish sex gland, indicating that TBC could cause obvious endocrine disruption. Therefore, it is needed to characterize the toxicity of heterocyclic brominated flame retardant (BFRs), such as TBC, as they may cause potential contamination to aquatic ecosystems. |
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