Khursigara Alexis J, Ackerly Kerri Lynn, Esbaugh Andrew J
Marine Science Department, The University of Texas at Austin Marine Science Institute, 750 Channel View Dr, Port Aransas, TX 78373, United States of America; Department of Biological Sciences, Advanced Environmental Research Institute, University of North Texas, 1155 Union Cir, Denton, TX 76203, United States of America.
Marine Science Department, The University of Texas at Austin Marine Science Institute, 750 Channel View Dr, Port Aransas, TX 78373, United States of America. Electronic address: https://twitter.com/KerriAckerlyPhD.
Comp Biochem Physiol C Toxicol Pharmacol. 2022 Sep;259:109397. doi: 10.1016/j.cbpc.2022.109397. Epub 2022 Jun 24.
Crude oil and the constituent polycyclic aromatic hydrocarbons (PAHs) induce a consistent suite of sub-lethal effects in early life stage fishes. It has been suggested that 3-ring PAHs drive cardiotoxicity and that all other impacts are downstream consequences of these cardiac effects. However, recent studies have documented behavioral alterations that may not be linked to cardiotoxicity. This raises the question of whether the 3-ring PAHs that drive cardiotoxicity are also responsible for the observed neurological impairments. To explore this question, we exposed embryonic red drum (Sciaenops ocellatus) - a species that exhibits greater sensitivity to craniofacial malformations than cardiotoxicity - to individual 2-ring, 3-ring, and 4-ring PAHs for 48 h after which they were assessed for sub-lethal developmental malformations. No effects were observed following exposure to naphthalene, anthracene, dibenzothiophene, phenanthrene and fluorene at doses equivalent to the ΣPAH effective concentration 50 for craniofacial malformation in red drum. Conversely, pyrene caused complete lethality at the original dose, and a 5× diluted dose resulted in significantly reduced brain size and spine length. Similar sub-lethal effects were also observed in chrysene at the 1× dose. These results indicate that 4-ring PAHs are driving malformations in developing red drum and suggest oil induced impairments in this species are not a downstream consequence of 3-ring PAH induced cardiac malformations.
原油及其成分多环芳烃（PAHs）会在幼鱼早期生活阶段引发一系列持续的亚致死效应。有人提出，三环PAHs会导致心脏毒性，而所有其他影响都是这些心脏效应的下游后果。然而，最近的研究记录了一些可能与心脏毒性无关的行为改变。这就提出了一个问题，即导致心脏毒性的三环PAHs是否也应对观察到的神经损伤负责。为了探究这个问题，我们将胚胎红鼓鱼（眼斑拟石首鱼）——一种对颅面畸形比对心脏毒性更敏感的物种——暴露于单个二环、三环和四环PAHs中48小时，之后对它们进行亚致死发育畸形评估。在暴露于相当于红鼓鱼颅面畸形的ΣPAH有效浓度50的萘、蒽、二苯并噻吩、菲和芴剂量下，未观察到任何影响。相反，芘在原始剂量下导致完全致死，5倍稀释剂量导致脑尺寸和脊柱长度显著减小。在1倍剂量的 Chrysene中也观察到了类似的亚致死效应。这些结果表明，四环PAHs正在导致发育中的红鼓鱼出现畸形，并表明该物种中油诱导的损伤不是三环PAH诱导的心脏畸形的下游后果。
