Induction of oxidative stress and related transcriptional effects of perfluorononanoic acid using an in vivo assessment
- Authors
- Yang, S., Liu, S., Ren, Z., Jiao, X., and Qin, S.
- ID
- ZDB-PUB-140123-17
- Date
- 2014
- Source
- Comparative biochemistry and physiology. Toxicology & pharmacology : CBP 160: 60-65 (Journal)
- Registered Authors
- Keywords
- Apoptosis, Fatty acid β-oxidation, Oxidative stress, Perfluorononanoic acid, Zebrafish
- MeSH Terms
-
- Animals
- Dose-Response Relationship, Drug
- Enzyme Activation/drug effects
- Enzyme Activation/physiology
- Female
- Fluorocarbons/toxicity*
- Lipid Peroxidation/drug effects
- Lipid Peroxidation/physiology*
- Male
- Oxidative Stress/drug effects
- Oxidative Stress/physiology*
- Transcription, Genetic/drug effects
- Transcription, Genetic/physiology*
- Zebrafish
- PubMed
- 24295853 Full text @ Comp. Biochem. Physiol. C Toxicol. Pharmacol.
Perfluorononanoic acid (PFNA) is an organic pollutant ubiquitous in the environment. However, the potential toxicity of PFNA remains largely unknown in teleost fish. This study defined the oxidative stress and related transcriptional effects of PFNA at various concentrations on zebrafish larvae. Activities of superoxide dismutase were induced in PFNA-treated groups but attenuated with exposure to higher concentration. Catalase activity and lipid peroxidation were significantly inhibited or increased at the highest concentration, respectively. To test the apoptotic pathway, several genes related to cell apoptosis were examined using real-time PCR. The expression of p53, apoptosis-inducing factor (AIF) and c-Jun NH (2)-terminal kinase (JNK) was partially increased, while Bcl-2, an anti-apoptotic gene, was reduced, with no significant effects on Bax and caspase-3 during the exposure period. The effect of PFNA on lipid β-oxidation system was investigated by examining the activity of peroxisome fatty acyl-COA oxidase (ACOX) and the expression of peroxisome proliferating activating receptors (PPARs). ACOX activity was moderately elevated with marginal significance and was not a significant consequence of PPARα and PPARγ expression. The overall results suggest that turbulence of oxidative stress and apoptotic pathway is involved in PFNA-induced toxicity in zebrafish larvae, and the gene expression patterns are able to reveal some potential mechanisms of developmental toxicity.