The deleterious effects of ultraviolet radiation (UVR: 280 to 400 nm) on organisms inhabiting aquatic environments are determined by a combination of factors. The primary factor is the penetration of biologically effective radiation in the water column. Intensity and spectral composition of UVR at depth depend on physical (surface reflectance, sea state etc.) and chemical features such as dissolved organic material, pigment concentration and particle characteristics (Chapter 3). Secondly, the UVR exposure time of pelagic organisms depends on mixing phenomena, such as wind-induced vertical mixing (Chapter 4). Finally, the resultant UVR-stress will be determined by the vulnerability of the organisms to ultraviolet radiation and their capacity to ameliorate or prevent damage, for instance by repair processes, avoidance or the synthesis of UV-absorbing compounds (see Chapter 10).
Today it is generally believed that natural UVR is a strong environmental factor affecting both productivity and community structure in marine and fresh water ecosystems. In open marine waters, both UV-B (280 to 315 nm) and UV-A (315 to 400 nm) reduce phytoplankton primary production (see also Chapter 11) and bacterial production [1,2]. UVR has been demonstrated to influence the structure of marine and fresh water phytoplankton communities [3,4].
UV-B may damage essential molecules such as proteins [5,6], pigments [7,8] or DNA [9-12], This damage can potentially affect important cellular processes such as nutrient uptake [13,14], orientation and motility , photosynthesis [16-18] or DNA transcription and replication [19,20]. As a result, obstructed metabolic activity can cause decreased growth rates [21,22], reproduction  or mortality. The molecular target sites primarily affected in situ by UVR are thought to be DNA, the photosynthetic apparatus (for phototrophic organisms), or both. For example, in Antarctic ice algae, photosynthesis was shown to be affected via reduced PSII efficiency [24,25] or changes in the RUBISCO pool . A reduction in the performance of both steps in the process of photosynthesis will decrease the ability of a cell to photosynthesize, thereby hindering the carboxylation process. UV-B is strongly absorbed by DNA causing structural changes in these molecules that can interfere with vital cellular processes, such as DNA transcription and replication, resulting in mutations or cell death [19,27]. Furthermore, exposure of cells and tissues to UVR may generate indirect, oxidative DNA damage, mainly via the production of oxyradicals (see Chapter 8), leading to lesions such as strand breaks and DNA protein crosslinks. Up until a decade ago, nothing was known about the possibility of in situ DNA damage induction and accumulation in aquatic organisms. Karentz et al.  were the first to describe induction and repair of various DNA lesions following UV-B exposure. They showed large species specific differences in lesion induction in a variety of Antarctic marine diatoms (Figure 1), which was thought to be related with cell size. In those experiments UV-B was supplied using artificial UV-B (lamps) sources. In 1996, Jeffrey et al.  described, for the first time, the occurrence of UV-B-induced DNA damage in field samples of marine bacterio-plankton from the Gulf of Mexico. Since then, various studies have appeared concentrating on UV-B induced DNA lesions, mainly in the marine environment, but also in fresh water systems.
Although much is known now about the effects of solar radiation on the DNA of aquatic organisms, there are also a few major limitations in the presently available information. First, almost all studies have described the presence of cyclobutane pyrimidine dimers (CPDs) only. The main reason for this is that this type of lesion is formed at the highest frequency. Furthermore, CPDs are formed exclusively as a result of UV-B. CPDs are therefore suitable indicators for UV-B
0.0 0.1 0.2 0.3 0.4 0.5 0.6 0.7 surface area : volume ratio a. i-1-1-1-1-1 I |—
0.0 0.1 0.2 0.3 0.4 0.5 0.6 0.7 surface area : volume ratio
Figure 1. Relationship between surface area:volume ratios and total UV-B-induced photoproducts in 9 marine Antarctic diatoms. 1: Coscinodiscus oculis-iridis; 2: Corethron cryophilum\ 3: Odontella weissflogii; 4: Thalassiosira australis; 5: Chaetoceros convolutus; 6: Thalassiosira subtilis; 7: Chaetoceros socialis; 8: Chaetoceros neglectus; 9: Nitzschia kerguelensis. [Redrawn after Karentz et al. 9.]
stress and are also highly relevant for investigating effects of ozone depletion. Other lesions such as the pyrimidine (6-4) pyrimidone photoproduct (6-4 PP) and its Dewar isomer, however, may be formed by UV-B, although at lower rates. Little is known about the occurrence of these lesions, as they may occur in aquatic organisms under ambient solar radiation. In addition, other possible lesions induced by both UV-B and UV-A have not yet been investigated in aquatic organisms. In particular, UV-A can induce indirect, oxidative DNA damage resulting in single strand breaks (SBB), DNA-protein crosslinks, and 8-hydroxy-guanosine(8-oxoG). Clearly, the recent progress in UV effect research in aquatic systems is greatly restricted by the type of lesion under study. Secondly, the information that has become available over the past decade has been directed mainly to pelagic marine microorganisms, such as bacterio- and phytoplankton. Relatively little is known about possible lesion formation under natural irradiance conditions in higher organisms or in fresh water systems.
The aim of this chapter is to give an overview of the current knowledge on UV-B-induced effects on the DNA of aquatic organisms. It does not aim to fully summarize the DNA damage literature, but merely to put relevant data into an ecological perspective. For this reason, most of the emphasis will be given to available field data, which, to date, has been focused almost exclusively on CPDs induced by UV-B.
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