Concluding remarks

It is now evident that UV-B induced CPD accumulation is a general phenomenon in aquatic organisms. Viruses and bacteria are especially vulnerable to UV-B induced DNA damage. The small size of viruses and heterotrophic bacteria obviously favors CPD accumulation. The penetration of UV-B inside these cells is high, due to the lack of pigments, nuclear membranes or efficient UV screening by compounds such as MAAs, or, for viruses, the lack of photoreac-tivation potential. CPD accumulation in aquatic organisms may affect metabolic activity, growth, production, reproduction and viability. For example, Visser et al. [121] incubated sea water (<0.8 jum), consisting mainly of bacteria, in full solar radiation and demonstrated CPD induction over time, roughly following the UV-B dose. Simultaneously, reduction in bacterial production by UV-B was found to be correlated with the occurrence of DNA damage. Similar results were observed by Kase [125] within a single sample area but not between sample areas suggesting a lack of a universal relationship. For phytoplankton and other aquatic phototrophic organisms, such as macroalgae, CPD induction seems to mainly affect growth rate and not photosynthetic performance. Van de Poll et al. [73] showed a clear relationship between CPD accumulation and growth rate reduction for a range of red macrophytes. In contrast, effects of UV-B on variable fluorescence showed significantly different patterns. For phytoplankton, several studies (simulated in situ) have shown a different daily pattern for photoinhibition and CPD accumulation, indicating that these two processes are uncoupled. UV-mediated changes in the photosynthetic process, therefore, may not be indicative of DNA damage induction, or vice versa.

The importance of both excision repair [11,91,94] and photorepair [12,85,93,98] has been emphasized for a variety of aquatic microorganisms. In contrast, other studies have demonstrated minimal photorepair [94,96], Therefore, more studies on DNA repair processes are needed, but in particular the factors that influence photoreactivation capacity in situ. Several data sets, available for microbes, suggest that CPDs accumulate during the day in a roughly dose-dependent manner. This indicates that repair systems may be present but not very effective, especially in the afternoon. In contrast, in higher organisms [99,107] repair seems more efficient because daily patterns follow a more doserate dependent pattern showing significant decreases during afternoon hours. Very little is known about wavelength dependency of photoreactivation in aquatic organisms. Therefore biological weighting functions for photoreactivation in aquatic organisms and whole assemblages are urgently needed. Furthermore, very little is known about possible thresholds for photoreactivating irra-diance, or, more precisely, the dose (rate) dependency of photoreactivation. Therefore, dose-response relationships (UV-A/PAR versus repair rate) should be established for aquatic organisms.

Another factor that deserves further attention is the effect of UVR on viability. It seems from a limited number of field studies that UV-B causes viability loss in situ in a range of organisms (bacteria, phytoplankton, fish eggs). In fact the rather low repair rates that are established in incubation experiments could partly be explained by the presence of an unknown portion of non-viable organisms that have been killed during previous UV-B exposure events. In that respect photo-reactivation rates might be underestimated under in situ conditions because only a fraction of the CPDs is contained in viable cells may be capable of photoenzy-matic or other forms of repair. However, significant reduction in CPDs during dark periods, which could only be explained by active nucleotide excision repair [11], argue that viability may not be a dominant factor.

Finally, information on the induction and removal of lesions other than CPDs is urgently needed. Very little is known on the induction of the 6-4 PP in aquatic organisms, let alone the Dewar photoproduct. Furthermore, other lesions that may be induced by both UV-B and UV-A may be highly relevant. It is well known that UV-A may cause more than half of the total UVR effect, reducing primary and secondary production, both in marine and fresh water systems. It remains to be investigated whether or not the UV-A effect can be attributed to damage to photosystems alone (for phototrophs), or that other forms of oxidative damage are also important. The various pathways for ameliorating oxidative stress, such as the presence or induction of antioxidants, may be highly relevant as well.

DNA damage accumulates in every trophic level exposed to solar radiation. Because DNA damage accumulates in a range of trophic levels in marine and fresh water organisms very little can be concluded with respect to trophic consequences of DNA damage induction in aquatic organisms. Increased UV-B in the upper layer of the ocean might result in higher loss rates of viral infectivity. This may decrease the virus-induced mortality of bacteria and phytoplankton. On the other hand, bacteria and phytoplankton may be affected directly, so that primary and secondary production rates are depressed, although it has been found that UVR can change bacterioplankton community structure [109], assumably in favor of more UVR resistant species. Reduction of bacterial activity in the open oligotrophic ocean might have a strong impact on the microbial loop, because here production and remineralization are closely linked. Furthermore, as suggested by Davidson et al. [126] for an Antarctic marine system, changes in trophic interactions in marine organisms might strongly influence the biological pump. A reduction in bacterial activity might favor sedimentation of senescent diatoms, which would otherwise be broken down in the upper water layer. In this way, the biological pump would be stimulated. Moreover, as shown in several studies where shifts occurred in favor of diatoms, possibly as a result of a lower vulnerability for CPD induction, transportation of organic material could be enhanced as a result of (increased) UV-B. It is clear that the considerations given above are extremely speculative and without predictive meaning. In fact, many negative or positive feed back mechanisms can be envisioned, with all the potential feed-back loops that exist in aquatic food webs. Two approaches, therefore, seem to be logic options to proceed. The first one is a holistic approach where long-term effects of UVR on trophic structuring are considered, possibly in combination with molecular approaches to reveal phenomena of acclimation. The second one is ecosystem modeling, where a large number of parameters (including DNA damage accumulation and photoreac-tivation kinetics, production, growth) for various trophic levels and their interactive responses are incorporated.

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