Decreases in stratospheric ozone levels from anthropogenic inputs of chlorinated fluorocarbons have resulted in an increased amount of harmful ultraviolet-B (UVB, 290–320 nm) radiation reaching the sea surface in temperate latitudes (30–50 degrees N). In the Gulf of Maine, present-day irradiances of ultraviolet-A (UVA, 320–400 nm) radiation can penetrate to depths of 23 m and UVB radiation can penetrate to depths of 7–12 m, where the rapidly developing embryos and larvae of the Atlantic cod (Gadus morhua) are known to occur. Laboratory exposures of embryos and larvae of Atlantic cod to ultraviolet radiation (UVR) equivalent to a depth of approximately 10 m in the Gulf of Maine resulted in significant mortality of developing embryos and a decrease in standard length at hatching for yolk-sac larvae. Larvae at the end of the experimental period also had lower concentrations of UVR-absorbing compounds and exhibited significantly greater damage to their DNA, measured as cyclobutane pyrimidine dimer formation, after exposure to UVB radiation. Larvae exposed to UVB radiation also exhibited significantly higher activities and protein concentrations of the antioxidant enzyme superoxide dismutase and significantly higher concentrations of the transcriptional activator p53. p53 is expressed in response to DNA damage and can result in cellular growth arrest in the G1- to S-phase of the cell cycle or to programmed cell death (apoptosis). Cellular death caused by apoptosis is the most likely cause of mortality in embryos and larvae in these laboratory experiments, while the smaller size at hatching in those larvae that survived is caused by permanent cellular growth arrest in response to DNA damage. In addition, the sub-lethal energetic costs of repairing DNA damage or responding to oxidative stress may also contribute to poor individual performance in surviving larvae that could also lead to increases in mortality. The irradiances of UVB radiation that elicit these responses in cod larvae can occur in many temperate latitudes, where these ecologically and commercially important fish are known to spawn, and may contribute to the high mortality of cod embryos and larvae in their natural environment.
Octyl Methoxycinnamate Modulates Gene Expression and Prevents Cyclobutane Pyrimidine Dimer Formation but not Oxidative DNA Damage in UV-Exposed Human Cell Lines
