Our published studies have revealed that 2,2′,4,4′-tetrabromodiphenyl ether (BDE-47) could disrupt retina morphologies and related gene expressions of zebrafish larvae. Its possible effects on fish vision needed to be uncovered since sensory systems, especially eyes, are vital to wildlife. In this paper, two tests for vision development (opsin gene expression and photoreceptor immunostaining) and two tests for visually guided behaviors (optokinetic response and looming-evoked escape) were designed to investigate the potential visual impairments and subsequent ecological consequences caused by BDE-47 exposure in 6 dpf zebrafish larvae. The short wavelength sensitive cone opsins and rhodopsin were significantly inhibited by BDE-47 exposure. Meanwhile, BDE-47 exposure significantly reduced larval optokinetic responses with blue light stimuli and induced less larvae to exhibit escape response with looming stimuli, which confirmed the adverse consequences of visual impairments in zebrafish. Our results indicated that BDE-47 exposure impaired zebrafish larval vision (including color vision) development and further altered larval behaviors guided by vision, which provided adequate evidence to prove that the vision system was a novel and urgent toxicological target of environmental pollutants.

Proper visual function is essential for collecting environmental information and supporting the decision-making in the central nervous system and is therefore tightly associated with wildlife survival and human health. Polybrominated diphenyl ethers (PBDEs) were reported to impair zebrafish vision development, and thyroid hormone (TH) signaling was suspected as the main contributor. In this study, a pentabrominated PBDE, BDE-99, was chosen to further explore the action mechanism of PBDEs on the disruption of zebrafish color vision. The results showed that BDE-99 could impair multiple photoreceptors in the retina and disturb the behavior guided by the color vision of zebrafish larvae at 120 h post-fertilization. Although the resulting alteration in photoreceptor patterning highly resembled the effects of 3,3′,5-triiodo-L-thyroine, introducing the antagonist for TH receptors was unable to fully recover the alteration, which suggested the involvement of other potential regulatory factors. By modulating the expression of six7, a key inducer of middle-wavelength opsins, we demonstrated that six7, not THs, dominated the photoreceptor patterning in the disruption of BDE-99. Our work promoted the understanding of the regulatory role of six7 in the process of photoreceptor patterning and proposed a novel mechanism for the visual toxicity of PBDEs.

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