Tyrosinase inhibition prevents non-coplanar polychlorinated biphenyls and polybrominated diphenyl ethers-induced hyperactivity in developing zebrafish: Interaction between pigmentation and neurobehavior

IF 2.6 3区医学 Q3 NEUROSCIENCES

Neurotoxicology and teratology Pub Date : 2024-07-01 DOI:10.1016/j.ntt.2024.107373

Yasuaki Tanaka , Asako Shindo , Wenjing Dong , Tatsuro Nakamura , Kyoko Ogura , Kei Nomiyama , Hiroki Teraoka

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引用次数: 0

Abstract

Non-coplanar polychlorinated biphenyl (PCB) mixture Aroclor 1254 and polybrominated diphenyl ether (PBDE) BDE-47 are known to impede neurogenesis and neuronal development. We previously reported that exposure to PCB and PBDE leads to increased embryonic movement in zebrafish by decreasing dopamine levels. In this study, we studied the connection between the melanin and dopamine synthesis pathways in this context. Both genetic and chemical inhibition of tyrosinase, the rate-limiting enzyme in melanin synthesis, not only led to reduced pigmentation but also inhibit PCB/PBDE-induced embryonic hyperactivity. Furthermore, PCB and PBDE rarely affected tyrosinase expression in the potential pigment cells, suggesting that these compounds reduce dopamine through enzymatic regulation, including a competitive interaction for the substrate tyrosine. Our results provide new insights into the interactions between melanogenesis and dopaminergic neuronal activity, which may contribute to understanding the mechanisms underlying PCB/PBDE toxicity in developing organisms.

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抑制酪氨酸酶可防止非共面多氯联苯和多溴联苯醚诱发发育中斑马鱼的多动症：色素沉着与神经行为之间的相互作用

众所周知，非共面多氯联苯（PCB）混合物 Aroclor 1254 和多溴联苯醚（PBDE）BDE-47 会阻碍神经发生和神经元发育。我们以前曾报道过，暴露于多氯联苯和多溴联苯醚会降低多巴胺水平，从而导致斑马鱼胚胎运动增加。在这项研究中，我们研究了黑色素和多巴胺合成途径之间的联系。通过遗传和化学方法抑制黑色素合成过程中的限速酶--酪氨酸酶，不仅能减少色素沉着，还能抑制 PCB/PBDE 诱导的胚胎多动症。此外，多氯联苯和多溴联苯醚很少影响潜在色素细胞中酪氨酸酶的表达，这表明这些化合物通过酶调节减少多巴胺，包括对底物酪氨酸的竞争性相互作用。我们的研究结果为黑色素生成与多巴胺能神经元活动之间的相互作用提供了新的见解，这可能有助于理解多氯联苯/多溴联苯醚在发育中生物体内的毒性机制。

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来源期刊

Neurotoxicology and teratology 医学-毒理学

CiteScore

5.60

自引率

10.30%

发文量

审稿时长

58 days

期刊介绍： Neurotoxicology and Teratology provides a forum for publishing new information regarding the effects of chemical and physical agents on the developing, adult or aging nervous system. In this context, the fields of neurotoxicology and teratology include studies of agent-induced alterations of nervous system function, with a focus on behavioral outcomes and their underlying physiological and neurochemical mechanisms. The Journal publishes original, peer-reviewed Research Reports of experimental, clinical, and epidemiological studies that address the neurotoxicity and/or functional teratology of pesticides, solvents, heavy metals, nanomaterials, organometals, industrial compounds, mixtures, drugs of abuse, pharmaceuticals, animal and plant toxins, atmospheric reaction products, and physical agents such as radiation and noise. These reports include traditional mammalian neurotoxicology experiments, human studies, studies using non-mammalian animal models, and mechanistic studies in vivo or in vitro. Special Issues, Reviews, Commentaries, Meeting Reports, and Symposium Papers provide timely updates on areas that have reached a critical point of synthesis, on aspects of a scientific field undergoing rapid change, or on areas that present special methodological or interpretive problems. Theoretical Articles address concepts and potential mechanisms underlying actions of agents of interest in the nervous system. The Journal also publishes Brief Communications that concisely describe a new method, technique, apparatus, or experimental result.