Organisms have two main lines of defense against UVB: (1) avoidance of exposure (e.g., moving away from UVB, having external layers that block UVB transmission, synthesizing specific compounds that function as natural sunscreens); and (2) repair pathways that can recognize damage and either correct the UVB-induced defect or destroy the compromised molecules. While species have various combinations and efficiencies of these strategies, there is a high degree of similarity in UV defenses across prokaryotic and eukaryotic taxa. Life originated before the ozone layer formed and early organisms had to deal with more dangerous portions of the solar spectrum; thus, acquired effective defenses for avoiding or mitigating UV-induced damages have been retained. However, these highly conserved biological measures against UVB are not 100% successful. Nearly all organisms have a threshold limit for solar UV exposure.
Before organisms can take the obvious step to avoid UVB exposure, they must be able to detect the presence of UVB wavelengths. Many species can detect and respond to changing intensities of white (visible) light with positive or negative phototaxis, or physiological adjustments (e.g., induction of sunscreening compounds). While UVA vision is an important aspect of mate selection and feeding in some birds, fish, and insects, there are only a few reports of UVB vision. This may be related to lack of research in this area and past limitations of technology for measuring UVB fluences. UVB perception may be more widespread and new methods could provide more complete information.
Most protists, invertebrates, and vertebrates are capable of moving away from too bright levels of sunlight, thus avoiding excessive UVB exposure. Taking advantage of shade, burrowing, or swimming deeper into the water column will effectively reduce the dose of UVB received. Nonmotile organisms (e.g., plants, fungi, macroaglae) cannot make such adjustments and must rely on other mechanisms for sufficient protection.
The outer covering of any organism, such as hair, feathers, skin, shell, exoskeleton, cell wall, or only the cell membrane, serves as the first layer of protection against the environment. Many of these structures have evolved to minimize mechanical damage from physical stresses and predation pressure, but these external layers also serve to attenuate and often completely block the transmission of UVB before it can reach vital internal targets.
The majority of prokaryotic and eukaryotic species synthesize UV-absorbing compounds that can serve as natural sunscreens (Table 1). Many of these compounds are common across taxonomic groups and have multiple functions; they not only provide protection from UV, but can act as antioxidants, signal transducers, osmoregulators, structural components, etc. UV-absorbing compounds can be colorless substances (e.g. mycosporine-like amino acids) or pigments (e.g., melanin). Many are secondary metabolites produced via pathways involved with the synthesis of aromatic amino acids.
Table 1 Some of the common UV-absorbing compounds that serve as sunscreens and examples of representative taxa. Many of these compounds absorb most strongly in the UVA, but attenuate UVB wavelengths as well. Within each of these groups, some compounds also can act as antioxidants. Presence in a particular taxonomic group does not necessarily indicate the ability to synthesize the UV-absorbing compounds; animals often bioaccumulate UV protectants (e.g., MAAs, carotenoids)
Mycosporine-like amino acids (MAAs) Polyphenolics (includes flavinoids, phlorotannins) Pteridines
Widespread in prokaryotes and eukaryotes Widespread in prokaryotes and eukaryotes Cyanobacteria, algae, marine invertebrates, fish Plants, algae
Widespread in prokaryotes and eukaryotes
The generation of radicals by UVB interactions with aqueous solutions inside and outside of cells can be counteracted by the presence of antioxidants (Table 2). These compounds are capable of safely quenching ions before they oxidize DNA, proteins, and lipids. Several vitamins (e.g., A, C, E) and some enzymes (e.g., superoxide dismu-tase, catalase) play major roles in capturing and stabilizing free radicals in cells. Like the sunscreening molecules discussed above, antioxidants can often have multiple functions in cell metabolism.
A universal activity in cells is DNA repair, and there are several ways by which cells can identify and repair UVB-induced photoproducts. Nucleotide excision repair is the most common pathway and involves a suite of enzymes that can identify, remove, and replace damaged portions of DNA. Some taxa can directly reverse CPDs by photoreactivation, a process that requires the enzyme photolyase and the presence of UVA or visible light. Species might have a single or multiple repair pathways. An important factor in the successful mitigation of UVB effects is the balance between rates of DNA damage and repair.
Table 2 Examples of biological compounds involved in antioxidation
Superoxide dismutase (SOD) Ubiquinone (coenzyme Q) Uric acid Vitamin A (retinol) Vitamin C (ascorbic acid) Vitamin E (tocopherol)
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