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首页> 外文期刊>Journal of Experimental Marine Biology and Ecology >Hypersalinity as a trigger of seagrass (Thalassia testudinum) die-off events in Florida Bay: Evidence based on shoot meristem O_2 and H_2S dynamics
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Hypersalinity as a trigger of seagrass (Thalassia testudinum) die-off events in Florida Bay: Evidence based on shoot meristem O_2 and H_2S dynamics

机译：盐度过高引发佛罗里达湾海草死亡（Thalassia testudinum）死亡：基于分生组织O_2和H_2S动力学的证据

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The mechanisms initiating rapid, large-scale ( 50 km(2)) seagrass die-off events globally remain elusive. Thalassia testudinum, a dominant habitat-forming tropical seagrass of the Caribbean and tropical Atlantic region, experiences recurrent die-off events in Florida Bay. Thus, T. testudinum provides an excellent case study to identify triggers of large-scale seagrass mortality. Presently, seagrass die-off events in Florida Bay are correlated to high total sulfide (H2S, HS-, S2-) concentrations in the sediment porewater (= 2000 mu M), water column hypoxia, high temperature and hypersalinity (salinity 45). Because the mortality appears to be initiated at the shoot base within the meristem, we examined the response of shoot meristematic O-2 and H2S dynamics using microsensors over a 5-hour nighttime simulation. Shoots were held at salinity 35 (ambient) or 65 (hypersaline) using microsensors in intact cores with plants from the field. The rate of H2S intrusion in the dark and oxidation in the light were similar at 35 and 65 salinity. However, the tissue O-2 consumption rate was significantly higher under hypersaline conditions (-11.07 +/- 4.32 kPa pO(2) h(-1)) compared to ambient (-3.93 +/- 0.88 kPa pO(2) h(-1)) in the dark. Consequently, the meristematic pO(2) threshold (similar to 1.5 kPa O-2) where H2S intrusion occurred in the meristem was reached more rapidly, increasing the time H2S accumulated (1.5 to 2.8 h). Longer H2S accumulation time significantly increased maximum meristem H2S levels at 65 (536 +/- 330 mu M H2S) compared to 35 salinity (121 +/- 62 mu M H2S). These results in T. testudinum provide evidence for a triggering mechanism that links an enhanced respiratory rate under hypersaline conditions to sulfide toxicity. We propose that hypersalinity in Florida Bay, or any stressor that significantly increases nighttime respiration rates, can subject seagrasses to longer and higher concentrations of sulfide, a known phytotoxin, within the shoot meristem. This mechanism likely explains large-scale mass mortality of T. testudinum in Florida Bay during periods of high salinity and elevated porewater sulfide levels, although field experiments are required to further validate this supposition.
机译：全球范围内引发快速，大规模（> 50 km（2））海草死亡事件的机制仍然难以捉摸。加勒比海和热带大西洋地区的一种主要的栖息地形成热带海草-地中海藻（Thalassia testudinum），在佛罗里达湾经历了周期性的死亡事件。因此，T。testudinum为确定大规模海草死亡率的诱因提供了一个极好的案例研究。目前，佛罗里达湾海草的死亡事件与沉积物孔隙水（> = 2000μM），水柱缺氧，高温和高盐度（盐度> 45）中高的总硫化物（H2S，HS-，S2-）浓度相关。 ）。因为死亡率似乎是在分生组织内的芽基处开始的，所以我们在5小时的夜间模拟中使用微传感器检查了分生组织O-2和H2S动力学的响应。使用微传感器在田间植株完整的芯中将盐分保持在盐度35（环境温度）或65（高盐碱）下。在35和65的盐度下，黑暗中的H2S入侵速率和光中的氧化速率相似。但是，与环境（-3.93 +/- 0.88 kPa pO（2）h（）相比，高盐度条件下组织O-2的消耗速率（-11.07 +/- 4.32 kPa pO（2）h（-1））要高得多。 -1））在黑暗中。因此，更快地达到了分生组织中发生H2S入侵的分生组织pO（2）阈值（类似于1.5 kPa O-2），从而增加了H2S积累的时间（1.5至2.8小时）。与35盐度（121 +/- 62μMH2S）相比，更长的H2S累积时间显着增加了65（536 +/- 330μMH2S）的最大分生组织H2S水平。 T. testudinum中的这些结果为触发机制提供了证据，该机制将高盐条件下的呼吸频率增加与硫化物毒性联系起来。我们认为，佛罗里达湾的高盐度或任何显着增加夜间呼吸速率的压力源，都可使海草在分生组织内遭受更长和更高浓度的硫化物（一种已知的植物毒素）的侵害。这种机制可能解释了高盐度和孔隙水硫化物水平升高期间佛罗里达湾的睾丸三生的大规模大规模死亡，尽管需要进行现场试验来进一步验证这一假设。

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