PMID- 34971995
OWN - NLM
STAT- Publisher
LR  - 20231013
IS  - 1090-2414 (Electronic)
IS  - 0147-6513 (Linking)
VI  - 230
DP  - 2022 Jan 15
TI  - 2,4-dichlorophenol exposure induces lipid accumulation and reactive oxygen 
      species formation in zebrafish embryos.
PG  - 113133
LID - S0147-6513(21)01245-8 [pii]
LID - 10.1016/j.ecoenv.2021.113133 [doi]
AB  - 2,4-dichlorophenol (2,4-DCP) is commonly found in the aquatic environment that 
      can be formed by the conversion of triclosan, which is a high production volume 
      endocrine disturbing chemical. The study aims to understand the potential 
      developmental toxicity of 2,4-DCP by using the in vivo zebrafish. We exposed the 
      2,4-DCP to the zebrafish embryos and collected the samples at several selected 
      developmental stages (70-85% epiboly/10-12 somite/prim-5) for the whole mount in 
      situ hybridization. The staining is used to investigate the ventral patterning, 
      presumptive neural formation, and brain development. Results suggested that the 
      2,4-DCP exposure (up to 2.5 mg/L) did not affect the tested developmental 
      processes in the survived embryos. Further experiments on lipid accumulation and 
      oxidative stress were carried out at 5 days post fertilization larvae. Results 
      showed the accumulation of oil droplets and induction of reactive oxygen species 
      (ROS) in the larvae after the highest dosage exposure (2.5 mg/L). The real-time 
      qPCR results suggested that the alternation of lipid metabolism was due to the 
      reduced mRNA expressions of proliferator-activated receptor alpha (ppar-alpha) and 
      acetyl-CoA carboxylase (acc); while the suppressed glutathione peroxidase (gpx) 
      mRNA expression was responsible for the induction of the ROS. To conclude, the 
      study provided scientific merits of understanding 2,4-DCP toxicity, and suggested 
      the possible underlying mechanism of the defects.
CI  - Copyright (c) 2021. Published by Elsevier Inc.
FAU - Tsukazawa, Kazumi Sunny
AU  - Tsukazawa KS
AD  - Laboratory of Developmental Disorders and Toxicology, Center for Promotion of 
      International Education and Research, Faculty of Agriculture, Kyushu University, 
      Fukuoka, Japan.
FAU - Li, Lei
AU  - Li L
AD  - Guangdong Provincial Key Laboratory of Brain Connectome and Behavior, CAS Key 
      Laboratory of Brain Connectome and Manipulation, the Brain Cognition and Brain 
      Disease Institute (BCBDI), Shenzhen Institutes of Advanced Technology, Chinese 
      Academy of Sciences, Shenzhen-Hong Kong Institute of Brain Science-Shenzhen 
      Fundamental Research Institutions, Shenzhen 518055, PR China.
FAU - Tse, William Ka Fai
AU  - Tse WKF
AD  - Laboratory of Developmental Disorders and Toxicology, Center for Promotion of 
      International Education and Research, Faculty of Agriculture, Kyushu University, 
      Fukuoka, Japan. Electronic address: kftse@agr.kyushu-u.ac.jp.
LA  - eng
PT  - Journal Article
DEP - 20211228
PL  - Netherlands
TA  - Ecotoxicol Environ Saf
JT  - Ecotoxicology and environmental safety
JID - 7805381
SB  - IM
OTO - NOTNLM
OT  - Developmental toxicity
OT  - Embryogenesis
OT  - Environmental pollutant
OT  - Lipid metabolism
OT  - Oxidative stress
EDAT- 2022/01/01 06:00
MHDA- 2022/01/01 06:00
CRDT- 2021/12/31 20:21
PHST- 2021/11/02 00:00 [received]
PHST- 2021/12/17 00:00 [revised]
PHST- 2021/12/27 00:00 [accepted]
PHST- 2022/01/01 06:00 [pubmed]
PHST- 2022/01/01 06:00 [medline]
PHST- 2021/12/31 20:21 [entrez]
AID - S0147-6513(21)01245-8 [pii]
AID - 10.1016/j.ecoenv.2021.113133 [doi]
PST - ppublish
SO  - Ecotoxicol Environ Saf. 2022 Jan 15;230:113133. doi: 
      10.1016/j.ecoenv.2021.113133. Epub 2021 Dec 28.