Department of Environmental and Occupational Health Sciences, University of Washington, Seattle, WA 98105-6099, United States.
Aquat Toxicol. 2013 Sep 15;140-141:295-302. doi: 10.1016/j.aquatox.2013.06.010. Epub 2013 Jun 22.
The olfactory system of salmonids is sensitive to the adverse effects of metals such as copper and cadmium. In the current study, we analyzed olfactory-mediated alarm responses, epithelial injury and recovery, and a suite of olfactory molecular biomarkers encoding genes critical in maintaining olfactory function in juvenile coho salmon receiving acute exposures to cadmium (Cd). The molecular biomarkers analyzed included four G-protein coupled receptors (GPCRs) representing the two major classes of odorant receptors (salmon olfactory receptor sorb and vomeronasal receptors svra, svrb, and gpr27), as well as markers of neurite outgrowth (nrn1) and antioxidant responses to metals, including heme oxygenase 1 (hmox1), and peroxiredoxin 1 (prdx1). Coho received acute (8-168 h) exposures to 3.7 ppb and 347 ppb Cd, and a subset of fish was analyzed following a 16-day depuration. Coho exposed to 347 ppb Cd over 48 h exhibited a reduction in freeze responses, and an extensive loss of olfaction accompanied by histological injury to the olfactory epithelium. The olfactory injury in coho exposed to 347 ppb Cd was accompanied at the gene level by significant decreases in expression of the olfactory GPCRs and increased expression of hmox1. Persistent behavioral deficits, histological injury and altered expression of a subset of olfactory biomarkers were still evident in Cd-exposed coho following a 16-day depuration in clean water. Exposure to 3.7 ppb Cd also resulted in reduced freeze responses and histological changes to the olfactory epithelium within 48 h of Cd exposure, although the extent of olfactory injury was less severe than observed for fish in the high dose Cd group. Furthermore adverse behavioral effects were present in some coho receiving the low dose of Cd following a 16-day depuration. In summary, acute exposures to environmental levels of Cd can cause olfactory injury in coho salmon that may persist following depuration. Mechanism-based biomarkers of oxidative stress and olfactory structures can augment the evaluation of olfactory injury manifested at the physiological level.
鲑鱼的嗅觉系统对铜和镉等金属的不良影响很敏感。在目前的研究中，我们分析了嗅觉介导的警报反应、上皮损伤和恢复，以及一系列关键的嗅觉分子生物标志物编码基因，这些基因在接受急性镉暴露的幼年银大麻哈鱼中维持嗅觉功能。分析的分子生物标志物包括代表两种主要气味受体（鲑鱼嗅觉受体 sorb 和 vomeronasal 受体 svra、svrb 和 gpr27）的四个 G 蛋白偶联受体 (GPCR)，以及神经突生长 (nrn1) 和金属抗氧化反应的标志物，包括血红素加氧酶 1 (hmox1) 和过氧化物酶 1 (prdx1)。银大麻哈鱼接受了急性（8-168 小时）暴露于 3.7 ppb 和 347 ppb 的 Cd，并且对一组鱼类进行了 16 天的净化分析。暴露于 347 ppb Cd 超过 48 小时的银大麻哈鱼表现出冻结反应减少，并且嗅觉上皮广泛丧失嗅觉，同时伴有组织学损伤。暴露于 347 ppb Cd 的银大麻哈鱼的嗅觉损伤在基因水平上伴随着嗅觉 GPCR 表达显著降低和 hmox1 表达增加。在清洁水中进行 16 天的净化后，暴露于 Cd 的银大麻哈鱼仍然表现出持续的行为缺陷、组织学损伤和嗅觉生物标志物的一部分表达改变。暴露于 3.7 ppb Cd 也导致在暴露于 Cd 后的 48 小时内冻结反应和嗅觉上皮的组织学变化，尽管嗅觉损伤的程度比高剂量 Cd 组中的鱼观察到的要轻。此外，在经过 16 天的净化后，一些接受低剂量 Cd 的银大麻哈鱼也表现出不利的行为影响。总之，急性暴露于环境水平的 Cd 会导致银大麻哈鱼的嗅觉损伤，并且在净化后可能会持续存在。基于氧化应激和嗅觉结构的机制生物标志物可以增强对在生理水平上表现出的嗅觉损伤的评估。
