期刊
ANTIOXIDANTS
卷 9, 期 8, 页码 -出版社
MDPI
DOI: 10.3390/antiox9080731
关键词
benzo[a]pyrene; neurotoxicity; oxidative stress; hypoxia-inducible factor
资金
- Ministry of Science and Technology, Taiwan [MOST 105-2313-B-415-001-, MOST 106-2313-B-415-001-, MOST 107-2313-B-415-001-]
Benzo[a]pyrene (B[a]P) is a polycyclic aromatic hydrocarbon formed by the incomplete combustion of organic matter. Environmental B[a]P contamination poses a serious health risk to many organisms because the pollutant may negatively affect many physiological systems. As such, chronic exposure to B[a]P is known to lead to locomotor dysfunction and neurodegeneration in several organisms. In this study, we used the zebrafish model to delineate the acute toxic effects of B[a]P on the developing nervous system. We found that embryonic exposure of B[a]P downregulatesshhandisl1, causing morphological hypoplasia in the telencephalon, ventral thalamus, hypothalamus, epiphysis and posterior commissure. Moreover, hypoxia-inducible factors (hif1aandhif2a) are repressed upon embryonic exposure of B[a]P, leading to reduced expression of the Hif-target genes,epoandsurvivin, which are associated with neural differentiation and maintenance. During normal embryogenesis, low-level oxidative stress regulates neuronal development and function. However, our experiments revealed that embryonic oxidative stress is greatly increased in B[a]P-treated embryos. The expression ofcatalasewas decreased andsod1expression increased in B[a]P-treated embryos. These transcriptional changes were coincident with increased embryonic levels of H(2)O(2)and malondialdehyde, with the levels in B[a]P-treated fish similar to those in embryos treated with 120-mu M H2O2. Together, our data suggest that reduced Hif signaling and increased oxidative stress are involved in B[a]P-induced acute neurotoxicity during embryogenesis.
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