Laboratorio de Limnología, INIBIOMA, CONICET-UNComahue , Bariloche, Argentina.
PLoS One. 2012;7(2):e32046. doi: 10.1371/journal.pone.0032046. Epub 2012 Feb 22.
Ultraviolet radiation (UVR) causes physical damage to DNA, carboxylation of proteins and peroxidation of lipids in copepod crustaceans, ubiquitous and abundant secondary producers in most aquatic ecosystems. Copepod adaptations for long duration exposures include changes in behaviour, changes in pigmentation and ultimately changes in morphology. Adaptations to short-term exposures are little studied. Here we show that short-duration exposure to UVR causes the freshwater calanoid copepod, Eudiaptomus gracilis, to rapidly activate production of enzymes that prevent widespread collateral peroxidation (glutathione S-transferase, GST), that regulate apoptosis cell death (Caspase-3, Casp-3), and that facilitate neurotransmissions (cholinesterase-ChE). None of these enzyme systems is alone sufficient, but they act in concert to reduce the stress level of the organism. The interplay among enzymatic responses provides useful information on how organisms respond to environmental stressors acting on short time scales.
紫外线辐射 (UVR) 会对甲壳类动物（桡足类）的 DNA 造成物理损伤，对蛋白质进行羧化，对脂质进行过氧化，桡足类是大多数水生生态系统中普遍存在且丰富的次级生产者。桡足类适应长时间暴露的方式包括行为改变、色素变化，最终是形态变化。对短期暴露的适应研究较少。在这里，我们表明，短时间暴露于 UVR 会导致淡水哲水蚤（Eudiaptomus gracilis）迅速激活产生防止广泛连锁过氧化的酶（谷胱甘肽 S-转移酶，GST），调节细胞凋亡（半胱天冬酶-3，Casp-3），并促进神经递质传递（胆碱酯酶-ChE）。这些酶系统都不是单独起作用的，但它们协同作用，降低了生物体的应激水平。酶反应之间的相互作用为生物体如何应对短时间尺度上的环境胁迫提供了有用的信息。
