Transmission of ultraviolet radiation through the Antarctic annual sea ice and its biological effects on sea urchin embryos

Stratospheric ozone depletion over Antarctica is expected to continue for the next 50 years, with increases in ecologically damaging ultraviolet radiation (UVR: 290–400 nm), specifically the ultraviolet-B (UVB: 290–320 nm) portion of the spectrum. Most of coastal Antarctica is covered with 2–3 m of annual sea ice during the occurrence of the ‘‘ozone hole.’’ This physical barrier to UVR transmission has long been assumed to provide complete protection from the biologically damaging effects of UVR, especially for the planktonic developmental stages of the benthic invertebrate fauna. We found that short-wavelength UVB (down to 304 nm) is transmitted through the Austral spring annual ice of McMurdo Sound, and causes significant mortality and DNA damage in the embryos of the sea urchin Sterechinus neumayeri. Although mortality of sea urchin embryos has been reported for the open waters of the Antarctic, this is the first documentation of mortality and DNA damage for embryos under the annual sea ice. The degree of mortality and DNA damage was dependent on both year and depth, with higher mortality and DNA damage at 1 m depth below the ice compared to 3 m and 5 m. Greater DNA damage occurred in 2003 compared to 2002 despite the thicker annual ice (3.1 m vs. 2.5 m). Although the thickness of the annual ice was greater, the severity of the ozone hole, 230 Dobson units (DU) versus 320 DU, and the ratio of UVB to visible radiation was greater in 2003. Embryo and larval mortality from exposure to UVR under the annual ice should be considered as another abiotic factor potentially affecting the temporally episodic recruitment of invertebrates that occur in this benthic ecosystem. In Antarctica the springtime depletion of stratospheric ozone (Hofmann et al. 1997; Soloman 1999) results in high irradiances of ultraviolet-B (290–320 nm) radiation (UVB) (Smith 1989, Madronich et al. 1998), and causes a decrease in primary productivity (Smith et al. 1992; Neale et al. 1998). The destruction of stratospheric ozone has been monitored since the early1980s and the biological effects of ultraviolet radiation (290–400 nm UVR) have been quantified for several trophic levels down to a depth of 20 m in open water (Karentz 1994). The harmful effects of UVR on marine organisms include damage to proteins, lipids, and DNA with both sublethal and lethal results. Of particular concern is that stratospheric ozone depletion results in an increase in damaging UVB wavelengths without a proportional increase in longer ultraviolet-A (UVA: 320–400 nm) and blue wavelengths involved in photoreactivation and photorepair (Smith 1989). The most common type of damage caused directly by UVR is DNA damage in the form of photolesions such as cyclobutane pyrimidine dimers (CPDs) and 6–4 photoproducts. The proportion of these products formed on DNA 1 Corresponding author ([email protected]). Acknowledgments We thank Michael Lombardi, Paul Brewin, Kate Schimanski, Angela Kopuris, and Brian Grant for technical and diving assistance. Dr. Toshio Mori generously supplied the monoclonal antibodies to CPD photoproducts. This project was supported by the National Science Foundation (Biological Oceanography and International Programs), the University of New Hampshire Marine Program, the University of Otago, and Antarctica New Zealand. by UVR is ;75% for CPDs and 25% for 6–4 photoproducts. To repair these DNA lesions organisms have evolved the enzyme photolyase, a light-dependent enzyme that requires UVA and visible irradiances (350 nm to 450 nm) to be catalytic (Kim and Sancar 1993). The proportionally lower irradiances of UVA and blue wavelengths that occur during the ‘‘ozone hole’’ could potentially change the balance between damage and repair processes in favor of damage under