Abstract
The 'ozone hole' has caused an increase in ultraviolet B radiation (UV-B, 280-320. nm) penetrating Antarctic coastal marine ecosystems, however the direct effect of this enhanced UV-B on pelagic organisms remains unclear. Oxidative stress, the in vivo production of reactive oxygen species to levels high enough to overcome anti-oxidant defences, is a key outcome of exposure to solar radiation, yet to date few studies have examined this physiological response in Antarctic marine species in situ or in direct relation to the ozone hole. To assess the biological effects of UV-B, in situ experiments were conducted at Cape Armitage in McMurdo Sound, Antarctica (77.06 degrees S, 164.42 degrees E) on the common Antarctic sea urchin Sterechinus neumayeri Meissner (Echinoidea) over two consecutive 4-day periods in the spring of 2008 (26-30 October and 1-5 November). The presence of the ozone hole, and a corresponding increase in UV-B exposure, resulted in unequivocal increases in oxidative damage to lipids and proteins, and developmental abnormality in embryos of S. neumayeri growing in open waters. Results also indicate that embryos have only a limited capacity to increase the activities of protective antioxidant enzymes, but not to levels sufficient to prevent severe oxidative damage from occurring. Importantly, results show that the effect of the ozone hole is largely mitigated by sea ice coverage. The present findings suggest that the coincidence of reduced stratospheric ozone and a reduction in sea ice coverage may produce a situation in which significant damage to Antarctic marine ecosystems may occur.