John Wiley & Sons, Ltd.

Comparison of PBDE congeners as inducers of oxidative stress in zebrafish

One of the proposed primary pathways through which PBDEs disrupt normal biological functions is oxidative stress. In this study, four PBDE congeners were evaluated for their potential to initiate oxidative stress in zebrafish during development: BDE 28, BDE 47, BDE 99, and BDE 100. N‐acetylcysteine (NAC) was used to increase intracellular GSH concentrations, and only decreased the effects of BDE 28 at 10 and 20 ppm, and BDE 47 at 20 ppm. NAC co‐exposure did not alter the rates of mortality or curved body axis as compared to PBDE exposure alone. The activity of GST was not altered at 24 hpf, but increased following 10 ppm BDE 28 exposure at 120 hpf. Transcription of several genes associated with stress was also evaluated. At 24 hpf, cox6a transcription was upregulated in embryos exposed to BDE 99, and BDE 28 exposure upregulated the transcription of gstpi. At 24 hpf, gclc was slightly downregulated by all congeners evaluated. At 120 hpf, trap1 and cox6a were upregulated by all congeners, however gstpi was downregulated by all congeners. The results of qRT‐PCR are mixed and do not strongly support a transcriptional response to oxidative stress. According to our data, PBDEs do not induce oxidative stress. Oxidative stress may occur at high exposure concentrations; however, this does not appear to be a primary mechanism of action for the PBDE congeners tested. This article is protected by copyright. All rights reserved

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