ORIGINAL RESEARCH
mRNA Expression of Select Hypoxia-Inducible Genes and Apoptotic Control Genes in Zebrafish Exposed to Hypoxia during Development
Zhonghai Ding1, Ping Sun1, Xin Hua1, Yiyao Bai1, Eva H. H. Shang2, Rudolf S. S. Wu2, Yuhui Zuo1
 
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1State Key Laboratory of Pollution Control and Resource Reuse, School of the Environment, Nanjing University,
Nanjing 210046, China
2Center for Coastal Pollution and Conservation, City University of Hong Kong, Hong Kong SAR, China
 
 
Pol. J. Environ. Stud. 2013;22(2):357-365
 
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ABSTRACT
Hypoxia is well known to occur in contaminated water environments, but it is still unclear about its effects on transcription of hypoxia-inducible genes and apoptotic control genes in zebrafish during development. In this study, the expression of select genes during zebrafish embryonic development was detected at mRNA level to investigate spatio-temporal changes of hypoxia-inducible genes and apoptosis control genes, as well as the correlation between these genes. Results showed that up-regulation of hypoxia-inducible factor 1 (HIF-1α) mRNA occurred within the first 2 h of exposure to hypoxia, followed by up-regulation of other hypoxia-inducible genes controlled by HIF-1α, such as erythropoietin and vascular endothelial growth factor. 48 hpf (the critical period for embryonic development, especially for the development of a cardiac system) and 40 dpf (the critical period for sex differentiation and development) were found to be the two sensitive windows to hypoxia, at which time significant changes in the mRNA expression of all selected hypoxia-inducible genes were clearly evident. A higher ratio of pro-apoptotic gene (Bax) vs. anti-apoptotic gene (Bcl-2) transcriptions was found in the head as compared with in the tail under hypoxia. A higher Bax/Bcl-2 ratio was found in hypoxic males than in hypoxic females, suggesting that hypoxia potentially favors the formation of testes by inducing apoptosis in ovaries during the hermaphroditism in zebrafish, which in turn causes a malebiased sex ratio.
eISSN:2083-5906
ISSN:1230-1485
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