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Hepatic oxidative stress, DNA damage and apoptosis in adult zebrafish following sub‐chronic exposure to BDE ‐47 and BDE ‐153
Author(s) -
Meng Shunlong,
Chen Xi,
Gyimah Eric,
Xu Hai,
Chen Jiazhang
Publication year - 2020
Publication title -
environmental toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.813
H-Index - 77
eISSN - 1522-7278
pISSN - 1520-4081
DOI - 10.1002/tox.22985
Subject(s) - zebrafish , oxidative stress , dna damage , catalase , apoptosis , diphenyl ether , comet assay , chemistry , polybrominated diphenyl ethers , reactive oxygen species , microbiology and biotechnology , biology , biochemistry , gene , dna , organic chemistry , pollutant
Polybrominated diphenyl ethers (PBDEs) are ubiquitous and prolific contaminant in both the abiotic and biotic environment because of the wide industrial applications of these chemicals. In the present study, the effects of 2,2′,4,4′‐tetrabrominateddiphenyl ether (BDE‐47) and 2,2′,4,4′,5,5′‐hexabromodiphenyl ether (BDE‐153) exposure on the induction of hepatic oxidative stress, DNA damage, and the expression of apoptosis‐related genes in adult zebrafish were investigated. The activities of antioxidant enzymes, such as catalase and superoxide dimutase, significantly increased when adult zebrafish was exposed to various concentrations of BDE‐47 and BDE‐153 for 7 and 15 days. BDE‐47 and BDE‐153 elicited significant alterations in zebrafish 7‐Ethoxyresorufin‐ O ‐deethylase activity at 3, 7, or 15 days of exposure. In addition, the significant increase in comet assay parameters of zebrafish hepatocytes in a concentration‐dependent manner indicated BDE‐47 and BDE‐153 induced DNA damage, probably due to observed oxidative stress. Furthermore, a monotonically upregulation of p53 and Caspase3 , which are apoptotic‐regulated genes, and decreased expression ratio of the anti‐apoptotic B‐cell lymphoma/leukaemia‐2 and Bcl2‐associated X protein genes for all BDE‐47 and BDE‐153 treatments at 7 and 15 days indicated apoptosis induction in zebrafish liver. Our findings help elucidate the mechanisms of BDE‐47‐ and BDE‐153‐induced toxicity in zebrafish hepatocytes.