Glass Benjamin H, Barott Katie L
Department of Biology, University of Pennsylvania, Philadelphia, PA 19104, USA.
J Exp Biol. 2025 Jun 15;228(12). doi: 10.1242/jeb.250372. Epub 2025 Jun 27.
Anthropogenic pollution is driving an increase in the frequency and severity of seawater hypoxic events in coastal marine ecosystems. Although hypoxia decreases physiological performance in coral and sea anemone (phylum Cnidaria) larvae, the underlying cellular mechanisms remain unexplored. Here, larvae of the reef-building corals Galaxea fascicularis and Porites astreoides and the estuarine sea anemone Nematostella vectensis were exposed to normoxia or a simulated hypoxic event (6 h at <2 mg dissolved O2 l-1), and their metabolomic response was quantified at the end of the exposure period using targeted liquid chromatography-mass spectrometry. Baseline metabolite profiles (81 amino acids, acylcarnitines, organic acids and nucleotides) were broadly divergent between the three species, with the corals displaying a reliance on nitrogen cycling through amino acid metabolism, whereas N. vectensis relied on nucleotide metabolism. By contrast, several changes in metabolite abundances under hypoxia were shared (e.g. increases in lactate) and suggest the upregulation of glycolysis, lactic acid fermentation and fatty acid β-oxidation as conserved mechanisms for energy production under hypoxia. Changes in these pathways were correlated with adverse physiological outcomes, including conserved declines in swimming behavior and growth. Importantly, life history traits affecting metabolism influenced hypoxia responses. For example, P. astreoides larvae, which possess algal endosymbionts, displayed the least severe metabolic response to hypoxia among these species, possibly owing to symbiont resources. Overall, these findings demonstrate that hypoxia disrupts metabolic performance in coral and sea anemone larvae through conserved and divergent pathways, emphasizing the need to limit drivers of ocean deoxygenation.
人为污染正导致沿海海洋生态系统中海水缺氧事件的频率和严重程度不断增加。尽管缺氧会降低珊瑚和海葵（刺胞动物门）幼虫的生理性能，但其潜在的细胞机制仍未得到探索。在这里，造礁珊瑚束状星孔珊瑚和阿氏孔珊瑚的幼虫以及河口海葵星状海葵暴露于常氧环境或模拟缺氧事件（溶解氧低于2毫克/升，持续6小时），并在暴露期结束时使用靶向液相色谱 - 质谱法定量它们的代谢组学反应。三种物种之间的基线代谢物谱（81种氨基酸、酰基肉碱、有机酸和核苷酸）差异很大，珊瑚显示出依赖通过氨基酸代谢进行氮循环，而星状海葵则依赖核苷酸代谢。相比之下，缺氧条件下几种代谢物丰度的变化是共有的（例如乳酸增加），这表明糖酵解、乳酸发酵和脂肪酸β-氧化的上调是缺氧时能量产生的保守机制。这些途径的变化与不良生理结果相关，包括游泳行为和生长的持续下降。重要的是，影响代谢的生活史特征影响了缺氧反应。例如，拥有藻类内共生体的阿氏孔珊瑚幼虫在这些物种中对缺氧的代谢反应最不严重，这可能归因于共生体资源。总体而言，这些发现表明缺氧通过保守和不同的途径破坏珊瑚和海葵幼虫的代谢性能，强调了限制海洋脱氧驱动因素的必要性。
