Living in flowing water increases resistance to ultraviolet B radiation.

Ultraviolet B radiation (UV-B) is an important environmental driver that can affect locomotor performance negatively by inducing production of reactive oxygen species (ROS). Prolonged regular exercise increases antioxidant activities, which may alleviate the negative effects of UV-B-induced ROS. Animals naturally performing exercise, such as humans performing regular exercise or fish living in flowing water, may therefore be more resilient to the negative effects of UV-B. We tested this hypothesis in a fully factorial experiment, where we exposed mosquitofish (Gambusia holbrooki) to UV-B and control (no UV-B) conditions in flowing and still water. We show that fish exposed to UV-B and kept in flowing water had increased sustained swimming performance (Ucrit), increased antioxidant defences (catalase activity and glutathione concentrations) and reduced cellular damage (lipid peroxidation and protein carbonyl concentrations) compared with fish in still water. There was no effect of UV-B or water flow on resting or maximal rates of oxygen consumption. Our results show that environmental water flow can alleviate the negative effects of UV-B-induced ROS by increasing defence mechanisms. The resultant reduction in ROS-induced damage may contribute to maintain locomotor performance. Hence, the benefits of regular exercise are 'transferred' to improve resilience to the negative impacts of UV-B. Ecologically, the mechanistic link between responses to different habitat characteristics can determine the success of animals. These dynamics have important ecological connotations when river or stream flow changes as a result of weather patterns, climate or human modifications.

UV-B exposure reduces locomotor performance by impairing muscle function but not mitochondrial ATP production.

Ultraviolet B radiation (UV-B) can reduce swimming performance by increasing reactive oxygen species (ROS) formation. High concentrations of ROS can damage mitochondria, resulting in reduced ATP production. ROS can also damage muscle proteins, thereby leading to impaired muscle contractile function. We have shown previously that UV-B exposure reduces locomotor performance in mosquitofish (Gambusia holbrooki) without affecting metabolic scope. Our aim was therefore to test whether UV-B influences swimming performance of mosquitofish by ROS-induced damage to muscle proteins without affecting mitochondrial function. In a fully factorial design, we exposed mosquitofish to UV-B and no-UV-B controls in combination with exposure to N-acetylcysteine (NAC) plus no-NAC controls. We used NAC, a precursor of glutathione, as an antioxidant to test whether any effects of UV-B on swimming performance were at least partly due to UV-B-induced ROS. UV-B significantly reduced critical sustained swimming performance and tail beat frequencies, and it increased ROS-induced damage (protein carbonyl concentrations and lipid peroxidation) in muscle. However, UV-B did not affect the activity of sarco-endoplasmic reticulum ATPase (SERCA), an enzyme associated with muscle calcium cycling and muscle relaxation. UV-B did not affect ADP phosphorylation (state 3) rates of mitochondrial respiration, and it did not alter the amount of ATP produced per atom of oxygen consumed (P:O ratio). However, UV-B reduced the mitochondrial respiratory control ratio. Under UV-B exposure, fish treated with NAC showed greater swimming performance and tail beat frequencies, higher glutathione concentrations, and lower protein carbonyl concentrations and lipid peroxidation than untreated fish. Tail beat amplitude was not affected by any treatment. Our results showed, firstly, that the effects of UV-B on locomotor performance were mediated by ROS and, secondly, that reduced swimming performance was not caused by impaired mitochondrial ATP production. Instead, reduced tail beat frequencies indicate that muscle of UV-B exposed fish were slower, which was likely to have been caused by slower contraction rates, because SERCA activities remained unaffected.

Plasticity of protective mechanisms only partially explains interactive effects of temperature and UVR on upper thermal limits.

Temperature and ultraviolet radiation (UVR) are key environmental drivers that are linked in their effects on cellular damage. Exposure to both high temperatures and UVR can cause cellular damage that result in the up-regulation of common protective mechanisms, such as the induction of heat shock proteins (Hsps) and antioxidants. As such, the interactive effects of these stressors at the cellular level may determine physiological limits, such as thermal tolerance. Furthermore, antioxidant activity is often thermally sensitive, which may lead to temperature dependent effects of UVR exposure. Here we examined the interactive effects of temperature and UVR on upper thermal limits, Hsp70 abundance, oxidative damage and antioxidant (catalase) activity. We exposed Limnodynastes peronii tadpoles to one of three temperature treatments (constant 18°C, constant 28°C and daily fluctuations between 18 and 28°C) in the presence or absence of UVR. Tadpoles were tested for upper thermal limits (CTmax), induction of Hsp70, oxidative damage and catalase activity. Our results show that CTmax was influenced by an interactive effect between temperature and UVR treatment. For tadpoles kept in cold temperatures, exposure to UVR led to cross-tolerance to high temperatures, increasing CTmax. Plasticity in this trait was not fully explained by changes in the lower level mechanistic traits examined. These results highlight the difficulty in predicting the mechanistic basis for the interactive effects of multiple stressors on whole animal traits. Multifactorial studies may therefore be required to understand how complex mechanistic processes shape physiological tolerances, and determine responses to environmental variation.

Ionocyte Immunolocalization and the Effects of Ultraviolet Radiation on Their Abundance and Distribution in the Alenins of Caspian Sea Salmon, Salmo trutta caspius.

OBJECTIVE: On a global scale, stratospheric ozone depletion has caused an increase in UV-B radiation reaching the earth's surface. Ultraviolet radiation has long been suspected to be harmful to aquatic organisms. MATERIALS AND METHODS: In order to study ionocyte localization (by Na(+)/K(+)-ATPase immunolocalization) and the effects of UV radiation on the ionocytes of skin and gills, the alevins of Salmo trutta caspius were exposed to different doses of UV radiation [unit low doses (ULD) of: 60 µw/cm(2) UVC; 100 µw/cm(2) UVB and 40 µw/cm(2) UVA and unit high doses (UHD) of: 90 µw/cm(2) UVC; 130 µw/cm(2) UVB and 50 µw/cm(2) UVA] using two adjustable F8T5 UV-B, 302 nm lamps (Japan) for 15 minutes once a day in laboratory conditions. Alevins not subjected to UV exposure served as a control group. RESULTS: In both UV exposure groups, all the alevins died on the ninth day. No mortality was observed in the control group. The Na(+)/K(+)-ATPase immunolocalization study indicated that ionocytes were located, in lessening order, on the yolk sac, trunk, gills, opercula and rarely on the head skin. Immunohistochemical results showed significant reduction in the number of ionocytes on the yolk sac, with lesser reduction on the trunk in both UV exposure groups. In contrast, the number of immunofluorescence cells on the gill was significantly elevated. Our results also showed that the size of ionocytes was reduced on the trunk and yolk sac in the UV exposure groups, but not significantly. Deformation and destruction of ionocytes on the yolk sac and trunk were observed with scanning electron microscope (SEM) in the UV exposure groups. CONCLUSION: Our results showed that ionocytes were located mainly on the yolk sac, in lesser amounts on the trunk, gills and opercula, and rarely also on the head skin of alevins. UV radiation caused deformation and reduction in the number and size of ionocytes on the trunk and yolk sac. As the skin cells of trout alevins possess essential functions for respiration, osmoregulation, excretion and defense during this stage of life, the observed damage may have contributed to their suddenly mortality in the UV exposure condition.