Department of Environmental Science and Analytical Chemistry, Stockholm University, Stockholm, Sweden.
Mass Spectrometry Laboratory, Center for Physical Science and Technology, Vilnius, Lithuania.
PLoS One. 2019 May 16;14(5):e0211304. doi: 10.1371/journal.pone.0211304. eCollection 2019.
Anthropogenic pressures, such as contaminant exposure, may affect stable isotope ratios in biota. These changes are driven by alterations in the nutrient allocation and metabolic pathways induced by specific stressors. In a controlled microcosm study with the amphipod Gammarus spp., we studied effects of the β-blocker propranolol on stable isotope signatures (δ15N and δ13C), elemental composition (%C and %N), and growth (protein content and body size) as well as biomarkers of oxidative status (antioxidant capacity, ORAC; lipid peroxidation, TBARS) and neurological activity (acetylcholinesterase, AChE). Based on the known effects of propranolol exposure on cellular functions, i.e., its mode of action (MOA), we expected to observe a lower scope for growth, accompanied by a decrease in protein deposition, oxidative processes and AChE inhibition, with a resulting increase in the isotopic signatures. The observed responses in growth, biochemical and elemental variables supported most of these predictions. In particular, an increase in %N was observed in the propranolol exposures, whereas both protein allocation and body size declined. Moreover, both ORAC and TBARS levels decreased with increasing propranolol concentration, with the decrease being more pronounced for TBARS, which indicates the prevalence of the antioxidative processes. These changes resulted in a significant increase of the δ15N and δ13C values in the propranolol-exposed animals compared to the control. These findings suggest that MOA of β-blockers may be used to predict sublethal effects in non-target species, including inhibited AChE activity, improved oxidative balance, and elevated stable isotope ratios. The latter also indicates that metabolism-driven responses to environmental contaminants can alter stable isotope signatures, which should be taken into account when interpreting trophic interactions in the food webs.
人为压力，如污染物暴露，可能会影响生物体内的稳定同位素比值。这些变化是由特定胁迫引起的营养分配和代谢途径的改变所驱动的。在一项使用桡足类生物 gammarus spp. 的受控微宇宙研究中，我们研究了β阻断剂普萘洛尔对稳定同位素特征（δ15N 和 δ13C）、元素组成（%C 和 %N）、生长（蛋白质含量和体型）以及氧化状态生物标志物（抗氧化能力、ORAC；脂质过氧化、TBARS）和神经活动（乙酰胆碱酯酶，AChE）的影响。基于普萘洛尔暴露对细胞功能的已知影响，即其作用模式（MOA），我们预计会观察到生长范围缩小，伴随着蛋白质沉积、氧化过程和 AChE 抑制减少，从而导致同位素特征增加。生长、生化和元素变量的观察到的反应支持了这些预测中的大多数。特别是，在普萘洛尔暴露中观察到了%N 的增加，而蛋白质分配和体型都下降了。此外，随着普萘洛尔浓度的增加，ORAC 和 TBARS 水平都降低了，TBARS 的降低更为明显，这表明抗氧化过程占主导地位。这些变化导致暴露于普萘洛尔的动物的 δ15N 和 δ13C 值与对照相比显著增加。这些发现表明，β阻断剂的 MOA 可用于预测非目标物种的亚致死效应，包括乙酰胆碱酯酶活性抑制、氧化平衡改善和稳定同位素比值升高。后者还表明，代谢驱动的对环境污染物的反应可以改变稳定同位素特征，在解释食物网中的营养相互作用时应考虑到这一点。
