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Sci Total Environ. 2014 Sep 1;491-492:271-8. doi: 10.1016/j.scitotenv.2014.03.129. Epub 2014 Apr 21.

Developmental toxicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin in artificially fertilized crucian carp (Carassius auratus) embryo.

Author information

  • 1School of Pharmacy, Sungkyunkwan University, Suwon, Gyeonggi-do 440-746, South Korea.
  • 2School of Pharmacy, Sungkyunkwan University, Suwon, Gyeonggi-do 440-746, South Korea. Electronic address: khchung@skku.edu.
  • 3Fusion Technology Laboratory, Hoseo University, Hoseoro 79, bungil 20, Baebang-myun, Asan, Chungnam 336-795, South Korea. Electronic address: ohsm0403@hoseo.edu.

Abstract

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a persistent bioaccumulative environmental contaminant that is an endocrine disruptor. Embryos of various fish species are responsive to TCDD and have been used as an alternative method to the acute toxicity test with juvenile and adult fish. The TCDD test has similar endpoints of developmental toxicity. However, their sensitivity and signs of TCDD-induced toxicity are different depending on fish species and its habit. Crucian carp (Carassius auratus) - the sentinel species for persistent organic pollutants and a common foodfish in China, Japan, and Korea - was used to identify the developmental toxicity of TCDD. We obtained the fertilized eggs from the artificial fertilization of crucian carp (97.45% success rate). Embryos at 3h post fertilization (hpf) were exposed to no vehicle, vehicle (dimethylsulfoxide, 0.1% v/v) or TCDD (0.128, 0.32, 0.8, 2 and 5 μg/L) for 1h and then fresh water was changed and aerated. Embryonic development and toxicity were monitored until 150 hpf. TCDD-exposed group showed no effects on embryo mortality and hatching rate from 6 to 126 hpf. On the other hand, the post-hatching mortality rate in TCDD-exposed group was increased in a dose-dependent manner, especially at high doses (0.8, 2 and 5 μg/L). The LD50 for larval mortality was calculated to 0.24 ng TCDD/g embryo. Pericardial edema was continuously observed in larvae of TCDD-exposed groups from hatching complete time (78 hpf), followed by the onset of yolk sac edema. Hemorrhage and edema showed a significant increase depending on exposure concentration and time. Expression of TCDD-related CYP1A genes was evaluated quantitatively. Embryo and larvae in TCDD-exposed groups displayed a significant increase of CYP1A gene expression. Overall, we defined TCDD-induced toxicity in artificially fertilized crucian carp embryo and these results suggest that crucian carp can be applied as an early life stage model of TCDD-induced toxicity.

Copyright © 2014 Elsevier B.V. All rights reserved.

KEYWORDS:

CYP1A; Crucian carp; Developmental toxicity; Early life stage; TCDD

PMID:
24751158
[PubMed - in process]
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